I. Critically Ill Patients
• Insulin therapy should be initiated for treatment of
persistent hyperglycemia, starting at a threshold of no
greater than 180 mg/dL (10.0 mmol/L).
• Once insulin therapy has been started, a glucose range
of 140 to 180 mg/dL (7.8 to 10.0 mmol/L) is recommended
for the majority of critically ill patients.
• Intravenous insulin infusions are the preferred method
for achieving and maintaining glycemic control in
critically ill patients.
• Validated insulin infusion protocols with demonstrated
safety and efficacy, and with low rates of occurrence
of hypoglycemia, are recommended.
• With IV insulin therapy, frequent glucose monitoring
is essential to minimize the occurrence of hypoglycemia
and to achieve optimal glucose control.
II. Noncritically Ill Patients
• For the majority of noncritically ill patients treated
with insulin, the premeal BG target should generally
be <140 mg/dL (<7.8 mmol/L) in conjunction with
random BG values <180 mg/dL (<10.0 mmol/L), provided
these targets can be safely achieved.
• More stringent targets may be appropriate in stable
patients with previous tight glycemic control.
• Less stringent targets may be appropriate in terminally
ill patients or in patients with severe comorbidities.
• Scheduled subcutaneous administration of insulin,
with basal, nutritional, and correction components, is
the preferred method for achieving and maintaining
glucose control.
• Prolonged therapy with SSI as the sole regimen is
discouraged.
• Noninsulin antihyperglycemic agents are not appropriate
in most hospitalized patients who require therapy
for hyperglycemia.
• Clinical judgment and ongoing assessment of clinical
status must be incorporated into day-to-day decisions
regarding treatment of hyperglycemia.
III. Safety Issues
• Overtreatment and undertreatment of hyperglycemia
represent major safety concerns.
• Education of hospital personnel is essential in engaging
the support of those involved in the care of inpatients
with hyperglycemia.
• Caution is required in interpreting results of POC glucose
meters in patients with anemia, polycythemia,
hypoperfusion, or use of some medications.
• Buy-in and financial support from hospital administration
are required for promoting a rational systems
approach to inpatient glycemic management.
IV. Cost
• Appropriate inpatient management of hyperglycemia
is cost-effective.
V. Discharge Planning
• Preparation for transition to the outpatient setting
should begin at the time of hospital admission.
• Discharge planning, patient education, and clear communication
with outpatient providers are critical for
ensuring a safe and successful transition to outpatient
glycemic management.
VI. Needed Research
• A selected number of research questions and topics for
guiding the management of inpatient hyperglycemia
in various hospital settings are proposed.
Friday, May 8, 2009
Thursday, April 16, 2009
Diagnosis of Cushing Syndrome: SUMMARY OF RECOMMENDATIONS
From: The Endocrine Society
3.0. DIAGNOSIS OF CUSHING’S SYNDROME
Who should be tested
3.1. We recommend obtaining a thorough drug history to
exclude excessive exogenous glucocorticoid exposure leading
to iatrogenic Cushing’s syndrome before conducting
biochemical testing (1 ).
3.2. We recommend testing for Cushing’s syndrome in the
following groups:
• Patients with unusual features for age (e.g. osteoporosis,
hypertension) (Table 1) (1 )
• Patients with multiple and progressive features,
particularly those who are more predictive of Cushing’s
syndrome (Table 1) (1 )
• Children with decreasing height percentile and increasing
weight (1 )
• Patients with adrenal incidentaloma compatible with
adenoma (1 ).
3.3. We recommend against widespread testing for Cushing’s
syndrome in any other patient group (1 ).
Initial testing
3.4. For the initial testing for Cushing’s syndrome, we
recommend one of the following tests based on its suitability
for a given patient (Fig. 1) (1 ):
3.4.1. Urine free cortisol (UFC; at least two measurements)
3.4.2. Late-night salivary cortisol (two measurements)
3.4.3. 1-mg overnight dexamethasone suppression test
(DST)
3.4.4. Longer low-dose DST (2 mg/d for 48 h)
3.5. We recommend against the use of the following to test for
Cushing’s syndrome (1 ):
• Random serum cortisol or plasma ACTH levels
• Urinary 17-ketosteroids
• Insulin tolerance test
• Loperamide test
• Tests designed to determine the cause of Cushing’s
syndrome (e.g. pituitary and adrenal imaging, 8 mg DST).
3.6. In individuals with normal test results in whom the
pretest probability is high (patients with clinical features
suggestive of Cushing’s syndrome and adrenal incidentaloma
or suspected cyclic hypercortisolism), we recommend further
evaluation by an endocrinologist to confirm or exclude the
diagnosis (1 ).
3.7. In other individuals with normal test results (in whom
Cushing’s syndrome is very unlikely), we suggest reevaluation
in 6 months if signs or symptoms progress (2 ).
3.8. In individuals with at least one abnormal test result (for
whom the results could be falsely positive or indicate
Cushing’s syndrome), we recommend further evaluation by an
endocrinologist to confirm or exclude the diagnosis
(1 ).
Subsequent evaluation
3.9. For the subsequent evaluation of abnormal initial test
results, we recommend performing another recommended test
(Fig. 1, 1 ).
3.9.1. We suggest the additional use of the dexamethasone-
CRH test or the midnight serum cortisol test in specific
situations (Fig. 1, 1 ).
3.9.2. We suggest against the use of the desmopressin
test, except in research studies, until additional data validate
its utility (2 ).
3.9.3. We recommend against any further testing for
Cushing’s syndrome in individuals with concordantly negative
results on two different tests (except in patients suspected of
having the very rare case of cyclical disease) (1 ).
3.9.4. We recommend tests to establish the cause of
Cushing’s syndrome in patients with concordantly positive
results from two different tests, provided there is no concern
regarding possible non-Cushing’s hypercortisolism (Table 2)
(1 ).
3.9.5. We suggest further evaluation and follow-up for
the few patients with concordantly negative results who are
suspected of having cyclical disease and also for patients with
discordant results, especially if the pretest probability of
Cushing’s syndrome is high (2 ).
4.0. SPECIAL POPULATIONS/CONSIDERATIONS
4.1. Pregnancy: We recommend the use of UFC and against
the use of dexamethasone testing in the initial evaluation of
pregnant women (1 ).
4.2. Epilepsy: We recommend against the use of
dexamethasone testing in patients receiving antiepileptic
drugs known to enhance dexamethasone clearance and
recommend instead measurements of nonsuppressed cortisol
in blood, saliva, or urine (1 ).
4.3. Renal failure: We suggest using the 1-mg overnight DST
rather than UFC for initial testing for Cushing’s syndrome in
patients with severe renal failure (2 ).
4.4. Cyclic Cushing’s syndrome: We suggest use of UFC or
midnight salivary cortisol tests rather than DSTs in patients
suspected of having cyclic Cushing’s syndrome (2 ).
4.5. Adrenal incidentaloma: We suggest use of the 1-mg DST
or late-night cortisol test, rather than UFC, in patients
suspected of having mild Cushing’s syndrome (2 ).
3.0. DIAGNOSIS OF CUSHING’S SYNDROME
Who should be tested
3.1. We recommend obtaining a thorough drug history to
exclude excessive exogenous glucocorticoid exposure leading
to iatrogenic Cushing’s syndrome before conducting
biochemical testing (1 ).
3.2. We recommend testing for Cushing’s syndrome in the
following groups:
• Patients with unusual features for age (e.g. osteoporosis,
hypertension) (Table 1) (1 )
• Patients with multiple and progressive features,
particularly those who are more predictive of Cushing’s
syndrome (Table 1) (1 )
• Children with decreasing height percentile and increasing
weight (1 )
• Patients with adrenal incidentaloma compatible with
adenoma (1 ).
3.3. We recommend against widespread testing for Cushing’s
syndrome in any other patient group (1 ).
Initial testing
3.4. For the initial testing for Cushing’s syndrome, we
recommend one of the following tests based on its suitability
for a given patient (Fig. 1) (1 ):
3.4.1. Urine free cortisol (UFC; at least two measurements)
3.4.2. Late-night salivary cortisol (two measurements)
3.4.3. 1-mg overnight dexamethasone suppression test
(DST)
3.4.4. Longer low-dose DST (2 mg/d for 48 h)
3.5. We recommend against the use of the following to test for
Cushing’s syndrome (1 ):
• Random serum cortisol or plasma ACTH levels
• Urinary 17-ketosteroids
• Insulin tolerance test
• Loperamide test
• Tests designed to determine the cause of Cushing’s
syndrome (e.g. pituitary and adrenal imaging, 8 mg DST).
3.6. In individuals with normal test results in whom the
pretest probability is high (patients with clinical features
suggestive of Cushing’s syndrome and adrenal incidentaloma
or suspected cyclic hypercortisolism), we recommend further
evaluation by an endocrinologist to confirm or exclude the
diagnosis (1 ).
3.7. In other individuals with normal test results (in whom
Cushing’s syndrome is very unlikely), we suggest reevaluation
in 6 months if signs or symptoms progress (2 ).
3.8. In individuals with at least one abnormal test result (for
whom the results could be falsely positive or indicate
Cushing’s syndrome), we recommend further evaluation by an
endocrinologist to confirm or exclude the diagnosis
(1 ).
Subsequent evaluation
3.9. For the subsequent evaluation of abnormal initial test
results, we recommend performing another recommended test
(Fig. 1, 1 ).
3.9.1. We suggest the additional use of the dexamethasone-
CRH test or the midnight serum cortisol test in specific
situations (Fig. 1, 1 ).
3.9.2. We suggest against the use of the desmopressin
test, except in research studies, until additional data validate
its utility (2 ).
3.9.3. We recommend against any further testing for
Cushing’s syndrome in individuals with concordantly negative
results on two different tests (except in patients suspected of
having the very rare case of cyclical disease) (1 ).
3.9.4. We recommend tests to establish the cause of
Cushing’s syndrome in patients with concordantly positive
results from two different tests, provided there is no concern
regarding possible non-Cushing’s hypercortisolism (Table 2)
(1 ).
3.9.5. We suggest further evaluation and follow-up for
the few patients with concordantly negative results who are
suspected of having cyclical disease and also for patients with
discordant results, especially if the pretest probability of
Cushing’s syndrome is high (2 ).
4.0. SPECIAL POPULATIONS/CONSIDERATIONS
4.1. Pregnancy: We recommend the use of UFC and against
the use of dexamethasone testing in the initial evaluation of
pregnant women (1 ).
4.2. Epilepsy: We recommend against the use of
dexamethasone testing in patients receiving antiepileptic
drugs known to enhance dexamethasone clearance and
recommend instead measurements of nonsuppressed cortisol
in blood, saliva, or urine (1 ).
4.3. Renal failure: We suggest using the 1-mg overnight DST
rather than UFC for initial testing for Cushing’s syndrome in
patients with severe renal failure (2 ).
4.4. Cyclic Cushing’s syndrome: We suggest use of UFC or
midnight salivary cortisol tests rather than DSTs in patients
suspected of having cyclic Cushing’s syndrome (2 ).
4.5. Adrenal incidentaloma: We suggest use of the 1-mg DST
or late-night cortisol test, rather than UFC, in patients
suspected of having mild Cushing’s syndrome (2 ).
Non- Classic CAH (Congential Adrenal Hyperplasia)
Question 1 Patient is tested for non-classic CAH in all these cases except:
1-Women with early hirsuitism including those with early premature adrenarche.
2- Women who have family history of CAH.
3- Women with hirsuitism and hyperkalemia.
4- Women with hirsuitism of from some ethnic groups with high CAH.
5- women with sudden new onset of hirsuitism after the age of 30.
The right answer is 5, all 1-4 are right indications to test for CAH. Although hirsuitism get worse with time in CAH, women with new onset sudden hisrutism at this age should be evaluated particularly for adrenal or ovarian tumors. Not all women with hirsuitims are tested for CAH since it is a rare cause of hirsuitism, the more common are polycystic ovaries and idiopathic. Every now and then you will find a woman who will not be satisfied with the diagnosis of idiopathic hirsuitism and you may need to test her for this diagnosis.
Question 2: in testing for non-classic CAH which is not true:
1- 17-OHP (17-hydroxyprogesterone) is greater than 82 ng/dl in children with this diagnosis.
2- 17-OHP is greater than 200 ng/dl in early follicular phase of women with this diagnosis.
3- 17 OHP greater than 1000 ng/dl 1 hour after 250 micrograms ACTH stimulation test confirms the diagnosis.
4- Genetic testing is important before starting treatment with dexamethazone.
The correct answer is 4. Though genotype and phenotype usually correlate most patients are diagnosed with 17-OHP response after ACTH as above. The increase in 17-OHP in this syndrome is due to the congenital deficiency of the enzyme 21- hydroxylase that convert 17 OHP to 11-deoxycortisol. Thus 17-OHP will be elevated and cause rise in androgens. 11 deoxycortisol is normally converted in the adrenal to cortisol and patients with CAH are severely deficient in cortisol in the classic or neonatal form and non or mildly so in the classic CAH. In neonatal form 17 OHP is in the thousands of ng/dl (normal newborns <100>
1-Women with early hirsuitism including those with early premature adrenarche.
2- Women who have family history of CAH.
3- Women with hirsuitism and hyperkalemia.
4- Women with hirsuitism of from some ethnic groups with high CAH.
5- women with sudden new onset of hirsuitism after the age of 30.
The right answer is 5, all 1-4 are right indications to test for CAH. Although hirsuitism get worse with time in CAH, women with new onset sudden hisrutism at this age should be evaluated particularly for adrenal or ovarian tumors. Not all women with hirsuitims are tested for CAH since it is a rare cause of hirsuitism, the more common are polycystic ovaries and idiopathic. Every now and then you will find a woman who will not be satisfied with the diagnosis of idiopathic hirsuitism and you may need to test her for this diagnosis.
Question 2: in testing for non-classic CAH which is not true:
1- 17-OHP (17-hydroxyprogesterone) is greater than 82 ng/dl in children with this diagnosis.
2- 17-OHP is greater than 200 ng/dl in early follicular phase of women with this diagnosis.
3- 17 OHP greater than 1000 ng/dl 1 hour after 250 micrograms ACTH stimulation test confirms the diagnosis.
4- Genetic testing is important before starting treatment with dexamethazone.
The correct answer is 4. Though genotype and phenotype usually correlate most patients are diagnosed with 17-OHP response after ACTH as above. The increase in 17-OHP in this syndrome is due to the congenital deficiency of the enzyme 21- hydroxylase that convert 17 OHP to 11-deoxycortisol. Thus 17-OHP will be elevated and cause rise in androgens. 11 deoxycortisol is normally converted in the adrenal to cortisol and patients with CAH are severely deficient in cortisol in the classic or neonatal form and non or mildly so in the classic CAH. In neonatal form 17 OHP is in the thousands of ng/dl (normal newborns <100>
Question 3 In treating non-classic CAH with glucocorticoids which is not true:
1- Dexamethazone is given in doses of 0.25 mg to 0.75 mg at bed time.
2- Most women and men with the disease will require glucocorticoids.
3- Glucocorticoids are given mainly to suppress ACTH secretion.
4- Cushing features and osteoporosis can result.
5- 17 OHP is used to monitor therapy.
The rigth answer is 2. Glucocorticoids are given mainly to suppress ACTH that would stimulate further synthesis of 17 OHP which would convert into androstendione that forms testosterone. It is given at night since the surge of ACTH occurs more overnight. Unlike the classic form where all patients need glucocorticoids as permanent replacement, in the non-classic form it is indicated only in females with anovulatory cycles that desire fertility, males with testicular mass or oligospermia desiring fertility. Women with non classic CAH with hirsuitism and acne are treated with oral contraceptives or anti-androgens. Patient with irregular periods are treated with contraceptive pills. The long term significant side effects of glucocorticoids even at mild doses preclude its use except mainly for the indications stated.
Treatment of Low HDL
By: Maged Taman
The National Cholesterol Education Program (Adult Treatment Program [ATP] III) guidelines, published in 2001, identified the following HDL cholesterol levels as high risk:
1- HDL less than 40 mg/dL (1.0 mmol/L)
2- For patients with the metabolic syndrome (insulin resistance syndrome or syndrome X), gender adjusted HDL-cholesterol levels of less than 40 mg/dL in men and 50 mg/dL in women.
ATP III recommends the following approach to the management of patients with low HDL :
The primary target of therapy is LDL cholesterol; this goal should be reached before treating low HDL cholesterol.
1- For all patients: intensify weight management, increase physical activity, and encourage smoking cessation.
2- When a low HDL is associated with high triglycerides (200 to 499 mg/dL [2.3 to 5.6 mmol/dL]), first achieve non-HDL goals. Thus the goal of LDL according to patient risk of cardiovascular disease.
3- If triglycerides are <200 name="32">Exercise
1- weight loss (in overweight subjects)
2- smoking cessation
3- substitution of monounsaturated for saturated fatty acids
4- Avoiding if possible medications that lower HDL-cholesterol (beta blockers and androgens)
5- Lipid lowering drugs: most effective nicotinc acid, fibrate and statin in this order. However the choice depend in the LDL levels and trigylcerides. Thus a statin is used if LDL is elevated and fibrate is used if triglyerides are elevated while in isolated low HDL nicotinc acid is the drug of choice.
Lipid lowering in Common clinical scenarios:
1- Patient with elevated LDL, normal triglycerides and low HDL: use statin to acheive LDL goal, HDL may go up some highest with crestor 10%. Nicotinc acid may be added if HDL is still low. Statin and Nicotinc acid combination cause slight increase in myopathy over statin alone.
2- If elevated LDL is accompanied with high triglycerides (200-499 mg/dl) and low HDL: statin is first started according to targeted cholesterol level, then if targets for triglycerides not achieved add fibrates. The lesser myopathy would be expected with combination of paravastatin and Fenofibrate (Tricor).
3- LDL is not elevated while triglyceride is elevated (200-499 mg/dl) with or without low HDL: Fibrate is the lipid lowering agent of choice in patients with CAD, strong family history of CAD or multiple risk factors for CAD.
4- LDL is minimally elevated while triglycerides is elevated (200-499 mg/dl) and low HDL: Fibrate is used for its main effect in triglycerides in this case and HDL. It may as well bring LDL to target. If still some elevation of LDL a statin can be added. Attentively, Ezetimibe or Bile acid sequestrant are used for statin intolerant patients.
5- Very high triglycerides (> 500 mg/dl): should be treaterd first and quickly by treating the cause as high blood sugar, stopping alcohol or drug like estrogen or tamoxifen. Meantime low fat diet and a fibrate shoud be started. Nicotnic acid may need to be added with good attention to potential rise of blood glucose. After triglyerides are lowered to less than 500 mg/dl and the risk of pancreatitis is prevented a LDL level should be addressed.
6- Isolated low HDL in high risk patients: Nicotinc acid is the drug of first choice. It raises HDL by about 30% , if goal not achieved adding fibrate like gemfibrozil may increase HDL by 45%. For patients who can not tolerate nictoinc acid gemfibrozil can be use alone. Statin like rosuvastatin (crestor) raises HDL by 10% can be considered as an add on to fenofibrate rather than gemfibrozil to minimize risk of myopathy.
The National Cholesterol Education Program (Adult Treatment Program [ATP] III) guidelines, published in 2001, identified the following HDL cholesterol levels as high risk:
1- HDL less than 40 mg/dL (1.0 mmol/L)
2- For patients with the metabolic syndrome (insulin resistance syndrome or syndrome X), gender adjusted HDL-cholesterol levels of less than 40 mg/dL in men and 50 mg/dL in women.
ATP III recommends the following approach to the management of patients with low HDL :
The primary target of therapy is LDL cholesterol; this goal should be reached before treating low HDL cholesterol.
1- For all patients: intensify weight management, increase physical activity, and encourage smoking cessation.
2- When a low HDL is associated with high triglycerides (200 to 499 mg/dL [2.3 to 5.6 mmol/dL]), first achieve non-HDL goals. Thus the goal of LDL according to patient risk of cardiovascular disease.
3- If triglycerides are <200 name="32">Exercise
1- weight loss (in overweight subjects)
2- smoking cessation
3- substitution of monounsaturated for saturated fatty acids
4- Avoiding if possible medications that lower HDL-cholesterol (beta blockers and androgens)
5- Lipid lowering drugs: most effective nicotinc acid, fibrate and statin in this order. However the choice depend in the LDL levels and trigylcerides. Thus a statin is used if LDL is elevated and fibrate is used if triglyerides are elevated while in isolated low HDL nicotinc acid is the drug of choice.
Lipid lowering in Common clinical scenarios:
1- Patient with elevated LDL, normal triglycerides and low HDL: use statin to acheive LDL goal, HDL may go up some highest with crestor 10%. Nicotinc acid may be added if HDL is still low. Statin and Nicotinc acid combination cause slight increase in myopathy over statin alone.
2- If elevated LDL is accompanied with high triglycerides (200-499 mg/dl) and low HDL: statin is first started according to targeted cholesterol level, then if targets for triglycerides not achieved add fibrates. The lesser myopathy would be expected with combination of paravastatin and Fenofibrate (Tricor).
3- LDL is not elevated while triglyceride is elevated (200-499 mg/dl) with or without low HDL: Fibrate is the lipid lowering agent of choice in patients with CAD, strong family history of CAD or multiple risk factors for CAD.
4- LDL is minimally elevated while triglycerides is elevated (200-499 mg/dl) and low HDL: Fibrate is used for its main effect in triglycerides in this case and HDL. It may as well bring LDL to target. If still some elevation of LDL a statin can be added. Attentively, Ezetimibe or Bile acid sequestrant are used for statin intolerant patients.
5- Very high triglycerides (> 500 mg/dl): should be treaterd first and quickly by treating the cause as high blood sugar, stopping alcohol or drug like estrogen or tamoxifen. Meantime low fat diet and a fibrate shoud be started. Nicotnic acid may need to be added with good attention to potential rise of blood glucose. After triglyerides are lowered to less than 500 mg/dl and the risk of pancreatitis is prevented a LDL level should be addressed.
6- Isolated low HDL in high risk patients: Nicotinc acid is the drug of first choice. It raises HDL by about 30% , if goal not achieved adding fibrate like gemfibrozil may increase HDL by 45%. For patients who can not tolerate nictoinc acid gemfibrozil can be use alone. Statin like rosuvastatin (crestor) raises HDL by 10% can be considered as an add on to fenofibrate rather than gemfibrozil to minimize risk of myopathy.
PCO
By: Maged Taman
Question 1- Diagnosis of PCO by INH criteria requires all except:
1- the presence of oligomenorrhea,
2- evidence of hyperandrogenism (clinical: acne/hisrsuitism/male type baldness or chemical: elevated testosterone level)
3- exclusion of other causes of hyperandrogenism and menstrual irregularity.
4- Poylcystic ovaries on US.
the right answer is 4. It in the Rotterdam criteria that PCO in ultrasound that is required. Two out of three of the following are required to make the diagnosis: oligomenorrhea, hyperandrogenism, and polycystic ovaries on ultrasound.
Question 2: in initial biochemical evaluation of the oligomenorrhea and/or hyperandrogenism all is required except:
1- Serum UCG
2- FSH
3- Prolactin
4- TSH
5- Total testosterone
6- 24 h urine cortisol.
The right answer is 6. 1 is first step to role out pregnancy. 2 will role out primary ovarian failure as a cause. 3 will role out prolacinoma as a cause, 4 will role out hypothyroidism as a cause. Total testosterone is measured to role out the rare cases of ovarian and adrenal tumors where the levels are likely to be high compared by PCO which will be mostly <150>
Question 1- Diagnosis of PCO by INH criteria requires all except:
1- the presence of oligomenorrhea,
2- evidence of hyperandrogenism (clinical: acne/hisrsuitism/male type baldness or chemical: elevated testosterone level)
3- exclusion of other causes of hyperandrogenism and menstrual irregularity.
4- Poylcystic ovaries on US.
the right answer is 4. It in the Rotterdam criteria that PCO in ultrasound that is required. Two out of three of the following are required to make the diagnosis: oligomenorrhea, hyperandrogenism, and polycystic ovaries on ultrasound.
Question 2: in initial biochemical evaluation of the oligomenorrhea and/or hyperandrogenism all is required except:
1- Serum UCG
2- FSH
3- Prolactin
4- TSH
5- Total testosterone
6- 24 h urine cortisol.
The right answer is 6. 1 is first step to role out pregnancy. 2 will role out primary ovarian failure as a cause. 3 will role out prolacinoma as a cause, 4 will role out hypothyroidism as a cause. Total testosterone is measured to role out the rare cases of ovarian and adrenal tumors where the levels are likely to be high compared by PCO which will be mostly <150>
Question 3: The use of metformin in PCO was found to do all of the below except:
1- Non or mild effect on improving hirsuitism.
2- Non or non-proven mild effect on endometrial protection.
3- moderate effect on restoring ovulation (4 times the placebo).
4- Non or mild effect in restoring fertility.
5- moderate effect in improving insulin resistance.
6- moderate Birth defects in women on the drug during pregnancy.
7- Fetal loss is less in women with PCO who are in metformin than placebo.
Right answer is 6. For 1 and 2 BCP are more effective. Though metformin reduces elevated testosterone level it is not effective in treating hirsusitism in these patients. For 3 and 4 weight loss and exercise are the primary approach if it fails clomiphine is the most effective. Metformin induces ovulation in PCO and was found to be effective in some studies in treating infertility in these women, but in other studies found ineffective, the consensus is it is not effective. Clomphine induces ovulation in about 80% of PCO patients and 50% conceive with it. the effect of metformin however in obese women with obese women with PCO and insulin resistance is favorable. It is considered safe in pregnancy from metanalysis of studies conducted so far. Fetal loss is less in women who get pregnant on metformin than placebo and women with PCO on metformin may need a contraception method if pregnancy is not desired.
Types of Lipid Disorders
By: Maged Taman
Type I hyperlipoproteinemia:
increase in chylomicrons.
Total cholesterol is normal with high triglycerides 2000-25000
A referigerated overnight sample shows one layer of creamy chylomicrons.
Is due to to absence of LPL activity or apo- C-II. Both are autosomal recessive.
May cause eruptive xanthomata, hepatosplenomegaly, lipemia retinalis, acute pancreatitis.
Type IIa: Familial hypercholesterolemia:
increase total cholesterol and LDL with normal triglycerides and HDL.
Total cholesterol is 275-500 in the heterozygous and >500 in the hemozygus.
second to defective LDL receptor. Autosomal dominant.
Present as premature CAD, tendinous xanthomas, xanthelsma, corneal arcus.
Faimial defective Apo B100 is a similar condition with lipid profile similar to the hemozygus above.
Type IIb: Combined Hyperlipidemia:
Increase LDL and VLDL
Total cholesterol is about 250-500 with trglycerides 250-750. with high LDL and low HDL.
gentic defect causing increase apo B 100. Autosmoal dominant.
Premature CAD.
Type III: Familial dysbetalipoproteinemia:
increase VLDL and IDL, VLDL-cholestrol to triglycerides is greater than 0.3 (normal rati is 0.2)
Both total cholestroal and trigylerides are about 250-500 range. with high LDL and normal HDL. it is autosomal recessive.
Beta-VLDL detected in agarose gel electrophoresis.
Autosomal recessive second to defective or absent apo E apo-E2 instead of apo E3 that lead to less clearance of chylomicrons remanants.
Patient present with tuberoeruptive xanthoma, plamar xanthoma.
Type IV: Familial hypertriglycerdemia:
Increase triglycerides (200-500 mg/dl) and commonly low HDL . Total cholesterol and LDL are normal.
Autosmal dominant Second to heterozygous mutation of LPL gene.
Causes increase risk of premature CAD.
Type V Mixed Hypertriglycerdemia:
increase in both Chylomicrons and VLDL
A refreigerated sample overnight will show two layers creamy supernatant from chylomicorns and lower turbid from VLDL.
Mostly secondary to partial type I due to partial LPL deficiency in patient with risk for increase triglyceride as obesity, ETOH, DM, hypothyroidism, nephrotic syndrome, estorgens or tamoxifen. Primary form is possibly due to defect on apo E.
May cause hepatosplenomgaly and eruptive xanthoma as type I
Type I hyperlipoproteinemia:
increase in chylomicrons.
Total cholesterol is normal with high triglycerides 2000-25000
A referigerated overnight sample shows one layer of creamy chylomicrons.
Is due to to absence of LPL activity or apo- C-II. Both are autosomal recessive.
May cause eruptive xanthomata, hepatosplenomegaly, lipemia retinalis, acute pancreatitis.
Type IIa: Familial hypercholesterolemia:
increase total cholesterol and LDL with normal triglycerides and HDL.
Total cholesterol is 275-500 in the heterozygous and >500 in the hemozygus.
second to defective LDL receptor. Autosomal dominant.
Present as premature CAD, tendinous xanthomas, xanthelsma, corneal arcus.
Faimial defective Apo B100 is a similar condition with lipid profile similar to the hemozygus above.
Type IIb: Combined Hyperlipidemia:
Increase LDL and VLDL
Total cholesterol is about 250-500 with trglycerides 250-750. with high LDL and low HDL.
gentic defect causing increase apo B 100. Autosmoal dominant.
Premature CAD.
Type III: Familial dysbetalipoproteinemia:
increase VLDL and IDL, VLDL-cholestrol to triglycerides is greater than 0.3 (normal rati is 0.2)
Both total cholestroal and trigylerides are about 250-500 range. with high LDL and normal HDL. it is autosomal recessive.
Beta-VLDL detected in agarose gel electrophoresis.
Autosomal recessive second to defective or absent apo E apo-E2 instead of apo E3 that lead to less clearance of chylomicrons remanants.
Patient present with tuberoeruptive xanthoma, plamar xanthoma.
Type IV: Familial hypertriglycerdemia:
Increase triglycerides (200-500 mg/dl) and commonly low HDL . Total cholesterol and LDL are normal.
Autosmal dominant Second to heterozygous mutation of LPL gene.
Causes increase risk of premature CAD.
Type V Mixed Hypertriglycerdemia:
increase in both Chylomicrons and VLDL
A refreigerated sample overnight will show two layers creamy supernatant from chylomicorns and lower turbid from VLDL.
Mostly secondary to partial type I due to partial LPL deficiency in patient with risk for increase triglyceride as obesity, ETOH, DM, hypothyroidism, nephrotic syndrome, estorgens or tamoxifen. Primary form is possibly due to defect on apo E.
May cause hepatosplenomgaly and eruptive xanthoma as type I
Hirsuitism
Question 1: In the process of evaluation of a patient with hirsuitism, which statment is false:
1-Total testesterone is less than 150 ng/dl in most patients with PCO
2-LH:FSH ratio is more than 3 is diagostic in patients with PCO.
3- Adrenal CT or MRI is indicated to role out adrenal androgen-secreting tumor if serum DHEA-s is > 700 mcg/dL .
4- A transvaginal ultrasound if serum total testesterone is > 150 ng/dL, and DHA is not significantly elevated.
5- Labroscopy is indicated if testesterone level is > 200 ng/dL with negative imaging of ovaries and adrenals to look for a small ovarian tumor (likely a hilus-cell tumor) that is too small to be detected by ultrasonography.
The right answer is 2, LH:FSH ratio used to one of the criteria to diagnose PCO however due to the pulsatility of LH as well findings of same ratio in some normal women the test is not helpful.
Most patients with PCO have mildly elevated or even normal testosterone level high level of 150 or more suggests ovarian or adrenal tumors. An elevated DHEA-s will suggest to adrenal tumor while a normal a DHEA will suggest ovarian tumor in this condition.
Question -2 In treatment of women with hirsuitism which is the wrong answer:
1-BCP is added if cosmetic measures and direct hair removal methods are commonly ineffective alone.
2-BCP may take more than 6 months to show effect in hirsuitism.
3- Anti-androgens typically spironolactone is added if BCP is not effective.
4- Avandia is effective in treating hirsuitism due to PCO.
5- Metformin have been shown to be effective in hirsuitism due to PCO.
6- Vaniqa cream for short course of 6 months will cure hirsuitism.
7- Flutamide to be avoided for hepatotoxicity.
The right answer is 6. BCP (Birth Control Pills) is the drug of choice if cosmetic measures are not effective alone. If it fails anti-androgens is added on or if used alone patient has to be in highly effective way of contraception since have effect on sex organs of male fetus. Typically spironolactone is used, flutamide has high risk of hepatoxicity. Cyproterone and finasteride are two other antiadnrogens. Though avandia (rosiglitzone) is effective in decreasing hirsuitism it cause weight gain and has a cardiovascular risk. Metformin in metanalysis of 8 studies found to be ineffective in diminishing hirsuitsim. Vaniqa cream will suppress hair growth temporarily and recurrence is common unless it is continued or BCP and anti-androgens are used as well.
LDL Pearls
By: Maged Taman
1- Adults 20 years old or more should have fasting lipid profile. If normal they can retested at least once every 5 years.
2- Lipid profile is fasting Total cholesterol, triglycerides, LDL (bad cholesterol and HDL (good cholesterol).
3- Lipid profile assessment:
Total cholesterol: <200>150 normal (preferable <100>140/90 or in blood pressure medicine.
Low HDL
Family history of premature CAD: father, brother or son <55>45 years old and women >55 years old.
HDL > 60 cancells one of the above risk factors.
5- CAD equivalents: these are other astherosclerotic manifestations that lead to same risks of CAD death and nonfatal MI like that of established CAD. They are:
peripheral vascular disease
Abdominal Aortic aneurysm.
Carotid artery disease.
Diabetes Mellitus.
10-year risk> 20%
6- LDL and non HDL goals:
CAD or CAD equivalents:
LDL goal is <100>100 or even >70
Non-HDL goal (total cholesterol - HDL) <130>130
drug for LDL > 130 and 10 year risk of 10-20%
Drug for LDL >160 and 10 year risk is <10> 160
Drug for LDL > 190
Non-HDL goal <190
7- Statins are the drug of choice for above patients decreases LDL 20-60%, resins 15-30 %, nicotinc acid 10-25 %, fibrates 5-20%, cholesterol absorption blocker Zetia 17%.
8- Patients with premature CAD and normal lipid profile: check LP (a), apo B and homocysteine.
1- Adults 20 years old or more should have fasting lipid profile. If normal they can retested at least once every 5 years.
2- Lipid profile is fasting Total cholesterol, triglycerides, LDL (bad cholesterol and HDL (good cholesterol).
3- Lipid profile assessment:
Total cholesterol: <200>150 normal (preferable <100>140/90 or in blood pressure medicine.
Low HDL
Family history of premature CAD: father, brother or son <55>45 years old and women >55 years old.
HDL > 60 cancells one of the above risk factors.
5- CAD equivalents: these are other astherosclerotic manifestations that lead to same risks of CAD death and nonfatal MI like that of established CAD. They are:
peripheral vascular disease
Abdominal Aortic aneurysm.
Carotid artery disease.
Diabetes Mellitus.
10-year risk> 20%
6- LDL and non HDL goals:
CAD or CAD equivalents:
LDL goal is <100>100 or even >70
Non-HDL goal (total cholesterol - HDL) <130>130
drug for LDL > 130 and 10 year risk of 10-20%
Drug for LDL >160 and 10 year risk is <10> 160
Drug for LDL > 190
Non-HDL goal <190
7- Statins are the drug of choice for above patients decreases LDL 20-60%, resins 15-30 %, nicotinc acid 10-25 %, fibrates 5-20%, cholesterol absorption blocker Zetia 17%.
8- Patients with premature CAD and normal lipid profile: check LP (a), apo B and homocysteine.
Saturday, April 11, 2009
Bronchial Carcinoid Tumors
All are true about bronchial carcinoids except:
1- arises from Kulchitsky cells one type of the neuroendocrine cells APUD.
2- Serum chromogranin A mild elevated.
3- Causes carinoid syndrome in less than 5%.
4- Causes acromegaly due to releasing GHRH.
5- Can cause Cushing second to the release of ectopic ACTH.
6- Silver stain is the gold standard to identify the tumors histologically.
7- CT lung will identify most of the tumors. MR with gado will show enhancement of T2 if CT can not distinguish them from vessels. Octreotide scan will show metastasis however these are rare and the scan picks up other tumors and granuloma.
8- In bronchoscopy the tumor have characteristic appearance.
9- Central carcionids are diagnosed by biopsy through bronchoscopy.
10- peripheral carcinoids are diagnosed by CT-guided transthoracic needle aspiration.
11- Treatment of choice is surgical excision with mediastinal lymph node resection.
12- Liver is the most common site of metastasis that are better image by MRI, resection would prolong survival.
13- In patient with more advanced disease the treatment of choice is somatostatin analogue.
All are correct except silver stain it used to be the common stain used in the past now the confirmatory immunohistochemical stain in diagnosing Carcinoids are NSE, synaptophysin and chromogranin. The tumors are commonly locally malignant and slowly growing with 10 years survival is over 80% atypical carinoids however tends to have worse prognosis. MRI of the liver will identify metastasis to the liver. Though carcinoids rarely metastasis less than 5%. The liver is the main site of their metastasis.
1- arises from Kulchitsky cells one type of the neuroendocrine cells APUD.
2- Serum chromogranin A mild elevated.
3- Causes carinoid syndrome in less than 5%.
4- Causes acromegaly due to releasing GHRH.
5- Can cause Cushing second to the release of ectopic ACTH.
6- Silver stain is the gold standard to identify the tumors histologically.
7- CT lung will identify most of the tumors. MR with gado will show enhancement of T2 if CT can not distinguish them from vessels. Octreotide scan will show metastasis however these are rare and the scan picks up other tumors and granuloma.
8- In bronchoscopy the tumor have characteristic appearance.
9- Central carcionids are diagnosed by biopsy through bronchoscopy.
10- peripheral carcinoids are diagnosed by CT-guided transthoracic needle aspiration.
11- Treatment of choice is surgical excision with mediastinal lymph node resection.
12- Liver is the most common site of metastasis that are better image by MRI, resection would prolong survival.
13- In patient with more advanced disease the treatment of choice is somatostatin analogue.
All are correct except silver stain it used to be the common stain used in the past now the confirmatory immunohistochemical stain in diagnosing Carcinoids are NSE, synaptophysin and chromogranin. The tumors are commonly locally malignant and slowly growing with 10 years survival is over 80% atypical carinoids however tends to have worse prognosis. MRI of the liver will identify metastasis to the liver. Though carcinoids rarely metastasis less than 5%. The liver is the main site of their metastasis.
Friday, April 10, 2009
Glucagonoma
All of the following are true about glucagnoma except:
1- The tumore arises from the alpha cells of the pancreas.
2- The tumor most often arise from the tail of the pancrease.
3- Necrolytic migratory erythema rash is specific to glucagonoma.
4- Glucagon level > 1000pg/ml is diagnostic.
5- CT abdomen with contrast is intial study for localization.
6- Endoscopic US of pancreas will help both the localization and obtaining biopsy of the tumor.
7- It is among endocrine tumors that is uniquely associated with venous thromboembolism.
All are true except 3, this rash can occur in other conditions, however it is commonly the clue to this rare diagnosis. Weight loss and diabetes mellitus are common as well. Neuropsychiatric symptoms are common. The diagnosis is usally established late after the tumor have metastasized. The diagnosis is usually made after the skin rash occured and glucagon level is commonly quite elevated > 500 the normal is 100 level can be at high normal in few patients. CT is usually the test ordered to localize the tumor and potential metastasis which are commonly to the liver. Octreotoide scan will also show the tumor and metastasis however rarely needed since the CT will visualize the tumor in most cases. The second study is usually through endoscopic US that can identify tumors and as well allow needle biopsy of the tumors in the pancreas. In the early cases with no metastasis surgical removal of the tumor is done. In hepatic predominant disease from metastasis resection of hepatic metastasis or hepatic artery embolization may be effective in slowing the disease. Octretoide is quite effective in controlling the symptoms however regress of tumor is not clearly shown. Alpha interferon and chemotherapy are other options. Disease is monitored regularly with serum glucagon and CT. It is not uncoomon to have 5 year survival of 50% in metastatic slowly progressing disease.
1- The tumore arises from the alpha cells of the pancreas.
2- The tumor most often arise from the tail of the pancrease.
3- Necrolytic migratory erythema rash is specific to glucagonoma.
4- Glucagon level > 1000pg/ml is diagnostic.
5- CT abdomen with contrast is intial study for localization.
6- Endoscopic US of pancreas will help both the localization and obtaining biopsy of the tumor.
7- It is among endocrine tumors that is uniquely associated with venous thromboembolism.
All are true except 3, this rash can occur in other conditions, however it is commonly the clue to this rare diagnosis. Weight loss and diabetes mellitus are common as well. Neuropsychiatric symptoms are common. The diagnosis is usally established late after the tumor have metastasized. The diagnosis is usually made after the skin rash occured and glucagon level is commonly quite elevated > 500 the normal is 100 level can be at high normal in few patients. CT is usually the test ordered to localize the tumor and potential metastasis which are commonly to the liver. Octreotoide scan will also show the tumor and metastasis however rarely needed since the CT will visualize the tumor in most cases. The second study is usually through endoscopic US that can identify tumors and as well allow needle biopsy of the tumors in the pancreas. In the early cases with no metastasis surgical removal of the tumor is done. In hepatic predominant disease from metastasis resection of hepatic metastasis or hepatic artery embolization may be effective in slowing the disease. Octretoide is quite effective in controlling the symptoms however regress of tumor is not clearly shown. Alpha interferon and chemotherapy are other options. Disease is monitored regularly with serum glucagon and CT. It is not uncoomon to have 5 year survival of 50% in metastatic slowly progressing disease.
Glucocorticoid-Remediable Aldosteronism
In Glucocorticoid-Remediable Aldosteronism (GRA) all are true except:
1- It is an autosomal dominant condition.
2- Patients commonly present before age of 21 years old with hypertension.
3- Family history may be obtained of GRA, brain aneurysms or intracranial hemorrhage.
4- It is due to increase production of ACTH-sensitive aldosterone in the zona fasciulata.
5- Aldosterone:renin ratio and hypokalemia are not as significant as in primary hyperaldosteronism.
6- It is primarily diagnosed with dexamthazone suppression test and the presence of elevated 18 hydroxycortisol and 18 oxocortisol.
7- It is well treatable with glucocorticoid or aldosterone receptor antagonist.
All are true except 6 the primary diagnosis now is with demonstration of the chimeric gene. It should be considered in patients with early hypertension, family history or early strokes <40>
1- It is an autosomal dominant condition.
2- Patients commonly present before age of 21 years old with hypertension.
3- Family history may be obtained of GRA, brain aneurysms or intracranial hemorrhage.
4- It is due to increase production of ACTH-sensitive aldosterone in the zona fasciulata.
5- Aldosterone:renin ratio and hypokalemia are not as significant as in primary hyperaldosteronism.
6- It is primarily diagnosed with dexamthazone suppression test and the presence of elevated 18 hydroxycortisol and 18 oxocortisol.
7- It is well treatable with glucocorticoid or aldosterone receptor antagonist.
All are true except 6 the primary diagnosis now is with demonstration of the chimeric gene. It should be considered in patients with early hypertension, family history or early strokes <40>
Craniopharyngioma
All are true about Craniopharyngioma except:
1- Arises from remnants of Rhathke pouch.
2- A cystic calcified lesion in CT is very suggestive of the tumor.
3- Is malignant with metastasis in 20%.
4- Primary treatment is surgery.
5- Edema along optic tract is common finding in MRI.
6- Both anterior and posterior pituitary can be affected.
All are true except 3 it is a benign tumor but has high recurrence rate that it is dealt with as locally malignant tumor. Histologically it can be cystic epithelia, epithelial islands with degenerative cysts or epithelial humps like the enamel of developing teeth. It rarely metastasizes. Surgery is commonly incomplete and is followed by radiation. Attempt of total or subtotal excision using microsurgery decreases recurrence but has high operative mortality and morbidity rates. Cyst aspiration or intracystic radiation or chemotherapy may be used for recreant cysts. Patients commonly present in childhood with delay growth and in adult age with sexual dysfunction of amenorrhea in females and erectile dysfunction in males. hypothyroidism, adrenal insufficiency increase prolactin and central DI can also occur. Headaches and change in vision due to pressure in the optic chiasma can also occur.
1- Arises from remnants of Rhathke pouch.
2- A cystic calcified lesion in CT is very suggestive of the tumor.
3- Is malignant with metastasis in 20%.
4- Primary treatment is surgery.
5- Edema along optic tract is common finding in MRI.
6- Both anterior and posterior pituitary can be affected.
All are true except 3 it is a benign tumor but has high recurrence rate that it is dealt with as locally malignant tumor. Histologically it can be cystic epithelia, epithelial islands with degenerative cysts or epithelial humps like the enamel of developing teeth. It rarely metastasizes. Surgery is commonly incomplete and is followed by radiation. Attempt of total or subtotal excision using microsurgery decreases recurrence but has high operative mortality and morbidity rates. Cyst aspiration or intracystic radiation or chemotherapy may be used for recreant cysts. Patients commonly present in childhood with delay growth and in adult age with sexual dysfunction of amenorrhea in females and erectile dysfunction in males. hypothyroidism, adrenal insufficiency increase prolactin and central DI can also occur. Headaches and change in vision due to pressure in the optic chiasma can also occur.
Tuesday, March 10, 2009
Resolving the Coronary Artery Disease Epidemic through Plant-Based Nutrition
By: Caldwell B. Esselstyn, Jr., MD
From the Cleveland Clinic Foundation, Cleveland, Ohio
Taking the Offensive
Figure 4--Coronary angiograms of right coronary artery before (left) and showing 30% improvement (right) following approximately 60 months of a plant-based diet and cholesterol-lowering medication.As I have reported earlier,28,29 a plant-based diet in conjunction with cholesterol-reducing medication eliminated progression of coronary artery disease over a 12-year period in patients with triple-vessel disease. Most of the 18 patients had experienced an earlier failed intervention of bypass surgery or angioplasty. All patients who maintained the diet achieved the cholesterol goal of less than 150 mg/dL and had no recurrent coronary events during the 12 years. At 5 years, angiography was repeated in most cases. By analysis of the stenosis percentage none had progression of disease, and 70% had selective regression.28 These data are compelling when one considers that the same group had experienced more than 49 coronary events during the 8 years before this study.28
The recent case of a colleague is particularly telling. During September and October of 1996, a 44-year-old surgical colleague experienced occasional chest discomfort, yet neither electrocardiogram, stress echocardiography, or thallium scanning found evidence of disease. While eating the typical American diet, he had a total cholesterol of 156 mg/dL and an LDL of 97 mg/dL. He was lean, non-diabetic, and normotensive, did not smoke, and had no family history of coronary disease. His lipoprotein (a) and homocysteine levels were normal. On November 18, 1996, after his surgical duties, he became acutely ill with pain in the left arm, jaw, and chest. Immediate coronary catheterization found all vessels to be normal except for the left anterior descending artery, the distal third of which was diseased. Enzymes confirmed a myocardial infarction. However, no intervention was deemed appropriate.
This patient was aware of my ongoing study and was curious for more information. He and his wife consulted me for an in-depth review of the plant-based diet and techniques of this arrest and reversal study. He became the personification of commitment to the plant-based diet. Over the next 32 months, without cholesterol-lowering drugs, he maintained a mean total cholesterol of 89 mg/dL and an LDL of 38 mg/dL. The repeat angiogram 32 months after his infarction showed that the disease was completely reversed. (Fig.1)
Even though many people might find a plant-based diet initially difficult to follow, every patient with the diagnosis of coronary artery disease should at the least be offered the option of this potentially curative arrest and reversal approach. As this young surgeon's case illustrates, our plant-based diet approach can achieve total disease arrest and selective regression even in advanced cases. This approach is particularly compelling because patients can take control over the disease that was destroying them. If traditional interventional cardiology is a rear-guard action, our arrest and reversal therapy can be likened to a military offensive against atherosclerosis.
Limitations of this study are its modest number of participants and lack of comparable controls. Nevertheless, its size permitted the caregiver an opportunity for frequent patient encounters. These interactions enabled 75% of participants to achieve profound lipid reduction, dietary goals, and relief of symptoms which continued to improve throughout the study's 12-year duration. Patients essentially served as their own controls often achieving profound angiographic reversal of disease as reviewed in the angiographic core laboratory. Fig. 1-4
In addition, Dr. Dean Ornish has reported both 1- and 5-year data that support a plant-based approach to control coronary artery disease.16
Above is a portion copied from the author article.
From the Cleveland Clinic Foundation, Cleveland, Ohio
Taking the Offensive
Figure 4--Coronary angiograms of right coronary artery before (left) and showing 30% improvement (right) following approximately 60 months of a plant-based diet and cholesterol-lowering medication.As I have reported earlier,28,29 a plant-based diet in conjunction with cholesterol-reducing medication eliminated progression of coronary artery disease over a 12-year period in patients with triple-vessel disease. Most of the 18 patients had experienced an earlier failed intervention of bypass surgery or angioplasty. All patients who maintained the diet achieved the cholesterol goal of less than 150 mg/dL and had no recurrent coronary events during the 12 years. At 5 years, angiography was repeated in most cases. By analysis of the stenosis percentage none had progression of disease, and 70% had selective regression.28 These data are compelling when one considers that the same group had experienced more than 49 coronary events during the 8 years before this study.28
The recent case of a colleague is particularly telling. During September and October of 1996, a 44-year-old surgical colleague experienced occasional chest discomfort, yet neither electrocardiogram, stress echocardiography, or thallium scanning found evidence of disease. While eating the typical American diet, he had a total cholesterol of 156 mg/dL and an LDL of 97 mg/dL. He was lean, non-diabetic, and normotensive, did not smoke, and had no family history of coronary disease. His lipoprotein (a) and homocysteine levels were normal. On November 18, 1996, after his surgical duties, he became acutely ill with pain in the left arm, jaw, and chest. Immediate coronary catheterization found all vessels to be normal except for the left anterior descending artery, the distal third of which was diseased. Enzymes confirmed a myocardial infarction. However, no intervention was deemed appropriate.
This patient was aware of my ongoing study and was curious for more information. He and his wife consulted me for an in-depth review of the plant-based diet and techniques of this arrest and reversal study. He became the personification of commitment to the plant-based diet. Over the next 32 months, without cholesterol-lowering drugs, he maintained a mean total cholesterol of 89 mg/dL and an LDL of 38 mg/dL. The repeat angiogram 32 months after his infarction showed that the disease was completely reversed. (Fig.1)
Even though many people might find a plant-based diet initially difficult to follow, every patient with the diagnosis of coronary artery disease should at the least be offered the option of this potentially curative arrest and reversal approach. As this young surgeon's case illustrates, our plant-based diet approach can achieve total disease arrest and selective regression even in advanced cases. This approach is particularly compelling because patients can take control over the disease that was destroying them. If traditional interventional cardiology is a rear-guard action, our arrest and reversal therapy can be likened to a military offensive against atherosclerosis.
Limitations of this study are its modest number of participants and lack of comparable controls. Nevertheless, its size permitted the caregiver an opportunity for frequent patient encounters. These interactions enabled 75% of participants to achieve profound lipid reduction, dietary goals, and relief of symptoms which continued to improve throughout the study's 12-year duration. Patients essentially served as their own controls often achieving profound angiographic reversal of disease as reviewed in the angiographic core laboratory. Fig. 1-4
In addition, Dr. Dean Ornish has reported both 1- and 5-year data that support a plant-based approach to control coronary artery disease.16
Above is a portion copied from the author article.
Friday, February 20, 2009
Out-of-Control Blood Sugar May Affect Memory
From: Your Total Health News.
February 19 (HealthDay News) -- A rise in blood sugar levels causes poorer brain function in people with type 2 diabetes, according to a study that included nearly 3,000 people aged 55 and older at 52 sites in Canada and the United States.
The participants, who were part of a larger study on cardiovascular risk in diabetes, underwent cognitive tests designed to measure several aspects of memory function. The researchers found that a 1 percent increase in A1C levels (average blood glucose levels over a period of two to three months) was associated with slightly lower scores on tests of psychomotor speed, global cognitive function, memory and multi-tasking.
However, no link was found between tests scores and daily blood glucose levels, which are measured by a fasting plasma glucose test.
The findings appear in the February issue of Diabetes Care.
"One of the little-known complications of type 2 diabetes is memory decline leading to dementia, particularly Alzheimer's disease," principal investigator Dr. Jeff Williamson, of Wake Forest University Baptist Medical Center, said in a news release from the university.
"This study adds to the growing evidence that poorer blood glucose control is strongly associated with poorer memory function and that these associations can be detected well before a person develops severe memory loss," he said.
Previous research has shown that people with diabetes are 1.5 times more likely than those without diabetes to experience cognitive decline and develop dementia.
Williamson said that "people with type 2 diabetes and their health-care providers need to be careful in situations where there is education and teaching about diabetes care, as patients may need a little more time to absorb and process information."
And he urged people with diabetes to "be open to having a family member periodically making sure they are keeping track of managing their diabetes through monitoring, diet, exercise and medication."
Wake Forest University Baptist Medical Center, news release, Feb. 11, 2009
February 19 (HealthDay News) -- A rise in blood sugar levels causes poorer brain function in people with type 2 diabetes, according to a study that included nearly 3,000 people aged 55 and older at 52 sites in Canada and the United States.
The participants, who were part of a larger study on cardiovascular risk in diabetes, underwent cognitive tests designed to measure several aspects of memory function. The researchers found that a 1 percent increase in A1C levels (average blood glucose levels over a period of two to three months) was associated with slightly lower scores on tests of psychomotor speed, global cognitive function, memory and multi-tasking.
However, no link was found between tests scores and daily blood glucose levels, which are measured by a fasting plasma glucose test.
The findings appear in the February issue of Diabetes Care.
"One of the little-known complications of type 2 diabetes is memory decline leading to dementia, particularly Alzheimer's disease," principal investigator Dr. Jeff Williamson, of Wake Forest University Baptist Medical Center, said in a news release from the university.
"This study adds to the growing evidence that poorer blood glucose control is strongly associated with poorer memory function and that these associations can be detected well before a person develops severe memory loss," he said.
Previous research has shown that people with diabetes are 1.5 times more likely than those without diabetes to experience cognitive decline and develop dementia.
Williamson said that "people with type 2 diabetes and their health-care providers need to be careful in situations where there is education and teaching about diabetes care, as patients may need a little more time to absorb and process information."
And he urged people with diabetes to "be open to having a family member periodically making sure they are keeping track of managing their diabetes through monitoring, diet, exercise and medication."
Wake Forest University Baptist Medical Center, news release, Feb. 11, 2009
Glycemic Goals Clarified: HbA1c Of 7% Still Ceiling: Three groups issue position statement.
From: Clinical Endocrinology News
MIRIAM E. TUCKER (Senior Writer)
A target hemoglobin A1c of less than 7% should remain the general goal for nonpregnant adults with diabetes, despite the recent results from three large randomized trials showing that intensive glucose lowering did not reduce the risks of cardiovascular disease in people with longstanding type 2 diabetes.
But glycemic targets that are either more or less stringent than that standard may be prudent for certain individuals with diabetes, according to a joint position statement issued by the American College of Cardiology, American Diabetes Association, and American Heart Association and published online in their respective journals: the Journal of the American College of Cardiology, Diabetes Care, and Circulation.
“The ADA/AHA/ACC position statement is very well thought out and very well articulated. The authors should be commended for their concise analysis of the available data,” Dr. J. Michael Gonzalez-Campoy, medical director and CEO, Minnesota Center for Obesity, Metabolism, and Endocrinology, said in an interview.
The three organizations conducted a careful reexamination of glycemic control guidelines in light of the findings from the Action to Control Cardiovascular Risk in Diabetes (ACCORD), the Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified Release Controlled Evaluation (ADVANCE), and the Veterans Affairs Diabetes Trial (VADT). All showed no significant reduction in cardiovascular outcomes with intensive glucose control, but the ACCORD caused particular concern—and was halted early—because it showed a 22% increase in mortality among subjects randomized to a strategy of very intensive glycemic control with a target HbA1c of less than 6% (N. Engl. J. Med. 2008;358:2545–9).
Still, “The evidence obtained from ACCORD, ADVANCE, and VADT does not suggest the need for major changes in glycemic control targets, but rather additional clarification of the language that has consistently stressed individualization,” Dr. Jay S. Skyler and his associates wrote (Diabetes Care 2009;32:187–92).
Those clarifications include:
▸ To prevent microvascular and neuropathic complications in people with both type 1 and type 2 diabetes, the HbA1c goal for nonpregnant adults in general remains less than 7%. This recommendation is based on robust data from long-term studies including the Diabetes Control and Complications Trial (DCCT) and the United Kingdom Prospective Diabetes Study (UKPDS).
The American Association of Clinical Endocrinologists (AACE), which was not part of the group issuing the statement, recommends aiming for an HbA1c level of 6.5% or less.
▸ The general HbA1c goal of less than 7% also “appears reasonable” for prevention of macrovascular disease among those with recent onset of diabetes, based on long-term follow-up of the DCCT and UKPDS cohorts.
▸ For selected individual patients, even lower HbA1c goals than the general goal of less than 7% might be reasonable, provided that this target can be achieved without significant hypoglycemia or other adverse effects of treatment. Such individuals might include those with short duration of diabetes, long life expectancy, and no significant cardiovascular disease. This recommendation was based on subgroup analyses of the DCCT, UKPDS, and the microvascular evidence from the ADVANCE trial.
▸ Conversely, less stringent HbA1c goals may be appropriate for patients with a history of severe hypoglycemia, limited life expectancy, advanced microvascular or macrovascular complications, or extensive comorbid conditions or those with longstanding diabetes in whom the general goal is difficult to attain despite diabetes self-management and education, appropriate glucose monitoring, and effective doses of multiple glucose-lowering agents, including insulin.
▸ For primary and secondary cardiovascular risk reduction in patients with diabetes, providers should continue to follow the evidence-based recommendations for blood pressure treatment, lipid-lowering with statins, aspirin prophylaxis, smoking cessation, and healthy lifestyle behaviors delineated in the ADA Standards of Medical Care in Diabetes (Diabetes Care 2008;31[suppl 1]:s12–54) and the AHA/ADA guidelines for primary CVD prevention (Circulation 2007;115?:114–26).
Dr. Gonzalez-Campoy, who serves on the AACE board of directors, agreed with the recommendations. “The ACCORD, ADVANCE, and VADT emphasize the need to individualize care. … The recent publications that show no benefit in cardiovascular outcomes with attempts at normalizing glycemic control were all done on people with [longstanding] type 2 diabetes. Therefore, these findings are not applicable to people with type 1 diabetes, nor do they apply to people with new-onset diabetes mellitus.”
“People with type 2 diabetes who may achieve normal A1c values with lifestyle changes alone, or with weight management, should not increase their A1c values,” Dr. Gonzalez-Campoy added.
Indeed, a substudy of VADT presented at the ADA's annual meeting in June suggested that individuals earlier in their history of type 2 diabetes had the most benefit of improved glycemic control, noted Dr. Daniel Einhorn, head of the Sharp Diabetes Treatment and Research Center, San Diego.
“The key is not to throw out the baby with the bathwater. The VADT and ACCORD suggest that some populations may not benefit from tight glycemic control and there may be risks associated with tight control in these same populations, i.e with cardiovascular disease and/or increased risk of hypoglycemia. This does not detract from the wealth of information that good glycemic control confers benefit on microvascular disease and, given a long enough window, cardiovascular disease,” said Dr. Einhorn, also on the AACE board of directors.
Dr. Einhorn is a consultant to Takeda, Eli Lilly, Amylin Pharmaceuticals, and Merck.
MIRIAM E. TUCKER (Senior Writer)
A target hemoglobin A1c of less than 7% should remain the general goal for nonpregnant adults with diabetes, despite the recent results from three large randomized trials showing that intensive glucose lowering did not reduce the risks of cardiovascular disease in people with longstanding type 2 diabetes.
But glycemic targets that are either more or less stringent than that standard may be prudent for certain individuals with diabetes, according to a joint position statement issued by the American College of Cardiology, American Diabetes Association, and American Heart Association and published online in their respective journals: the Journal of the American College of Cardiology, Diabetes Care, and Circulation.
“The ADA/AHA/ACC position statement is very well thought out and very well articulated. The authors should be commended for their concise analysis of the available data,” Dr. J. Michael Gonzalez-Campoy, medical director and CEO, Minnesota Center for Obesity, Metabolism, and Endocrinology, said in an interview.
The three organizations conducted a careful reexamination of glycemic control guidelines in light of the findings from the Action to Control Cardiovascular Risk in Diabetes (ACCORD), the Action in Diabetes and Vascular Disease: Preterax and Diamicron Modified Release Controlled Evaluation (ADVANCE), and the Veterans Affairs Diabetes Trial (VADT). All showed no significant reduction in cardiovascular outcomes with intensive glucose control, but the ACCORD caused particular concern—and was halted early—because it showed a 22% increase in mortality among subjects randomized to a strategy of very intensive glycemic control with a target HbA1c of less than 6% (N. Engl. J. Med. 2008;358:2545–9).
Still, “The evidence obtained from ACCORD, ADVANCE, and VADT does not suggest the need for major changes in glycemic control targets, but rather additional clarification of the language that has consistently stressed individualization,” Dr. Jay S. Skyler and his associates wrote (Diabetes Care 2009;32:187–92).
Those clarifications include:
▸ To prevent microvascular and neuropathic complications in people with both type 1 and type 2 diabetes, the HbA1c goal for nonpregnant adults in general remains less than 7%. This recommendation is based on robust data from long-term studies including the Diabetes Control and Complications Trial (DCCT) and the United Kingdom Prospective Diabetes Study (UKPDS).
The American Association of Clinical Endocrinologists (AACE), which was not part of the group issuing the statement, recommends aiming for an HbA1c level of 6.5% or less.
▸ The general HbA1c goal of less than 7% also “appears reasonable” for prevention of macrovascular disease among those with recent onset of diabetes, based on long-term follow-up of the DCCT and UKPDS cohorts.
▸ For selected individual patients, even lower HbA1c goals than the general goal of less than 7% might be reasonable, provided that this target can be achieved without significant hypoglycemia or other adverse effects of treatment. Such individuals might include those with short duration of diabetes, long life expectancy, and no significant cardiovascular disease. This recommendation was based on subgroup analyses of the DCCT, UKPDS, and the microvascular evidence from the ADVANCE trial.
▸ Conversely, less stringent HbA1c goals may be appropriate for patients with a history of severe hypoglycemia, limited life expectancy, advanced microvascular or macrovascular complications, or extensive comorbid conditions or those with longstanding diabetes in whom the general goal is difficult to attain despite diabetes self-management and education, appropriate glucose monitoring, and effective doses of multiple glucose-lowering agents, including insulin.
▸ For primary and secondary cardiovascular risk reduction in patients with diabetes, providers should continue to follow the evidence-based recommendations for blood pressure treatment, lipid-lowering with statins, aspirin prophylaxis, smoking cessation, and healthy lifestyle behaviors delineated in the ADA Standards of Medical Care in Diabetes (Diabetes Care 2008;31[suppl 1]:s12–54) and the AHA/ADA guidelines for primary CVD prevention (Circulation 2007;115?:114–26).
Dr. Gonzalez-Campoy, who serves on the AACE board of directors, agreed with the recommendations. “The ACCORD, ADVANCE, and VADT emphasize the need to individualize care. … The recent publications that show no benefit in cardiovascular outcomes with attempts at normalizing glycemic control were all done on people with [longstanding] type 2 diabetes. Therefore, these findings are not applicable to people with type 1 diabetes, nor do they apply to people with new-onset diabetes mellitus.”
“People with type 2 diabetes who may achieve normal A1c values with lifestyle changes alone, or with weight management, should not increase their A1c values,” Dr. Gonzalez-Campoy added.
Indeed, a substudy of VADT presented at the ADA's annual meeting in June suggested that individuals earlier in their history of type 2 diabetes had the most benefit of improved glycemic control, noted Dr. Daniel Einhorn, head of the Sharp Diabetes Treatment and Research Center, San Diego.
“The key is not to throw out the baby with the bathwater. The VADT and ACCORD suggest that some populations may not benefit from tight glycemic control and there may be risks associated with tight control in these same populations, i.e with cardiovascular disease and/or increased risk of hypoglycemia. This does not detract from the wealth of information that good glycemic control confers benefit on microvascular disease and, given a long enough window, cardiovascular disease,” said Dr. Einhorn, also on the AACE board of directors.
Dr. Einhorn is a consultant to Takeda, Eli Lilly, Amylin Pharmaceuticals, and Merck.
Tuesday, January 27, 2009
Feel Better, Live Longer
From: www.newsweek.com
By Dean Ornish M.D
What really works to make sustainable changes in diet and lifestyle? It's probably not what you think. In over 30 years of conducting clinical research, I've learned that the real keys are pleasure, joy and freedom, not willpower, deprivation and austerity. Joy of living is sustainable; fear of dying is not.
Why? Because life is to be enjoyed. There's no point in giving up something you enjoy unless you get something back that's even better, and quickly. When people eat more healthfully, exercise, quit smoking, manage stress better, and love more, they find that they feel so much better, so quickly, it reframes the reason for making these changes from fear of dying (too scary) or risk-factor modification (too boring) to joy of living. Fortunately, the latest studies show how dynamic and powerful are the mechanisms that control our health and well-being. When you exercise and eat right:
Your brain receives more blood flow and oxygen, so you become smarter, think more clearly, have more energy, and need less sleep. Two studies showed that just walking for three hours per week for only three months caused so many new neurons to grow that it actually increased the size of people’s brains!
Your face receives more blood flow, so your skin glows more and wrinkles less. You look younger and more attractive. In contrast, an unhealthy diet, chronic emotional stress and smoking reduce blood flow to your face so you age more quickly. Smoking accelerates aging because nicotine causes your arteries to constrict, which decreases blood flow to your face and makes it wrinkle prematurely. This is why smokers look years older than they really are and often have a gray pallor. Supermodel Christy Turlington, whose father died of lung cancer, has a wonderful Web site, which is a powerful antidote to the idea that smoking is beautiful.
Your sexual organs receive more blood, so you become more potent—this is how drugs like Viagra and Levitra work—but without the costs and side effects. In contrast, unhealthy lifestyle choices often lead to impotence. For example, half of men who smoke are impotent. Cigarettes are marketed in ways that make it seem as though you'll be sexy and beautiful, but they really make you ugly and impotent—how sexy is that?
Your genes change. In May, my colleagues and I at the nonprofit Preventive Medicine Research Institute and the University of California, San Francisco, published a study in the Proceedings of the National Academy of Sciences showing that changing your lifestyle changes your genes. Really. After only three months of following the lifestyle program described in my book, "The Spectrum," the expression of over 500 genes changed in men with early-stage prostate cancer. We found that genes associated with cancer, heart disease and inflammation were downregulated or "turned off" whereas protective genes were upregulated or "turned on." Craig Venter's pioneering work showed that one way to change your genes is to synthesize new ones. Our research is showing that another way to change your genes is to change your lifestyle.
Your telomeres get longer. Telomeres are the ends of our chromosomes that control how long we live. As telomeres become shorter, then cells age and die more quickly. In simple terms, as your telomeres get shorter, your life gets shorter.
Chronic emotional stress shortens your telomeres. My colleagues, Elissa Epel and Elizabeth Blackburn of the University of California, San Francisco, conducted a pioneering study of mothers who were caring for a child with a chronic illness. They found that the more stress the women reported experiencing, the shorter their telomeres. Women with the highest levels of perceived stress had telomeres shorter on average by the equivalent of at least one decade of additional aging compared to low-stress women.
One of the most interesting findings in this study was that the mothers' perceptions of stress were more important than what was objectively occurring in their lives. The researchers gave the women a questionnaire and asked them to rate on a three-point scale how stressed they felt each day, and how out of control their lives felt to them. The women who perceived that they were under heavy stress had significantly shortened and damaged telomeres compared with those who felt more relaxed. Conversely, some of the women who felt relaxed despite raising a disabled child had more normal-appearing telomeres.
In other words, if you feel stressed, you are stressed.
I wondered: if chronic stress can decrease telomerase (an enzyme that repairs and lengthens telomeres) and cause telomeres to age more quickly, could healthy lifestyle changes prevent this from occurring? It did. A few months ago, my colleagues and I (including Blackburn) published a study in The Lancet Oncology showing that the telomerase enzyme increased by almost one-third after only three months of making comprehensive lifestyle changes. This was the first study showing that any intervention, even drugs, can increase telomerase and, thus, telomere length. If a new drugs were shown to do this, it would be worth a billion dollars, but you can accomplish this benefit virtually for free, and in only three months, simply by changing your lifestyle.
So, knowing that what was once thought impossible can now be accomplished in only a few months may capture our imaginations and be a powerful motivator to make sustainable lifestyle changes. For many people, these are choices worth making—not just to live longer, but also to feel better.
By Dean Ornish M.D
What really works to make sustainable changes in diet and lifestyle? It's probably not what you think. In over 30 years of conducting clinical research, I've learned that the real keys are pleasure, joy and freedom, not willpower, deprivation and austerity. Joy of living is sustainable; fear of dying is not.
Why? Because life is to be enjoyed. There's no point in giving up something you enjoy unless you get something back that's even better, and quickly. When people eat more healthfully, exercise, quit smoking, manage stress better, and love more, they find that they feel so much better, so quickly, it reframes the reason for making these changes from fear of dying (too scary) or risk-factor modification (too boring) to joy of living. Fortunately, the latest studies show how dynamic and powerful are the mechanisms that control our health and well-being. When you exercise and eat right:
Your brain receives more blood flow and oxygen, so you become smarter, think more clearly, have more energy, and need less sleep. Two studies showed that just walking for three hours per week for only three months caused so many new neurons to grow that it actually increased the size of people’s brains!
Your face receives more blood flow, so your skin glows more and wrinkles less. You look younger and more attractive. In contrast, an unhealthy diet, chronic emotional stress and smoking reduce blood flow to your face so you age more quickly. Smoking accelerates aging because nicotine causes your arteries to constrict, which decreases blood flow to your face and makes it wrinkle prematurely. This is why smokers look years older than they really are and often have a gray pallor. Supermodel Christy Turlington, whose father died of lung cancer, has a wonderful Web site, which is a powerful antidote to the idea that smoking is beautiful.
Your sexual organs receive more blood, so you become more potent—this is how drugs like Viagra and Levitra work—but without the costs and side effects. In contrast, unhealthy lifestyle choices often lead to impotence. For example, half of men who smoke are impotent. Cigarettes are marketed in ways that make it seem as though you'll be sexy and beautiful, but they really make you ugly and impotent—how sexy is that?
Your genes change. In May, my colleagues and I at the nonprofit Preventive Medicine Research Institute and the University of California, San Francisco, published a study in the Proceedings of the National Academy of Sciences showing that changing your lifestyle changes your genes. Really. After only three months of following the lifestyle program described in my book, "The Spectrum," the expression of over 500 genes changed in men with early-stage prostate cancer. We found that genes associated with cancer, heart disease and inflammation were downregulated or "turned off" whereas protective genes were upregulated or "turned on." Craig Venter's pioneering work showed that one way to change your genes is to synthesize new ones. Our research is showing that another way to change your genes is to change your lifestyle.
Your telomeres get longer. Telomeres are the ends of our chromosomes that control how long we live. As telomeres become shorter, then cells age and die more quickly. In simple terms, as your telomeres get shorter, your life gets shorter.
Chronic emotional stress shortens your telomeres. My colleagues, Elissa Epel and Elizabeth Blackburn of the University of California, San Francisco, conducted a pioneering study of mothers who were caring for a child with a chronic illness. They found that the more stress the women reported experiencing, the shorter their telomeres. Women with the highest levels of perceived stress had telomeres shorter on average by the equivalent of at least one decade of additional aging compared to low-stress women.
One of the most interesting findings in this study was that the mothers' perceptions of stress were more important than what was objectively occurring in their lives. The researchers gave the women a questionnaire and asked them to rate on a three-point scale how stressed they felt each day, and how out of control their lives felt to them. The women who perceived that they were under heavy stress had significantly shortened and damaged telomeres compared with those who felt more relaxed. Conversely, some of the women who felt relaxed despite raising a disabled child had more normal-appearing telomeres.
In other words, if you feel stressed, you are stressed.
I wondered: if chronic stress can decrease telomerase (an enzyme that repairs and lengthens telomeres) and cause telomeres to age more quickly, could healthy lifestyle changes prevent this from occurring? It did. A few months ago, my colleagues and I (including Blackburn) published a study in The Lancet Oncology showing that the telomerase enzyme increased by almost one-third after only three months of making comprehensive lifestyle changes. This was the first study showing that any intervention, even drugs, can increase telomerase and, thus, telomere length. If a new drugs were shown to do this, it would be worth a billion dollars, but you can accomplish this benefit virtually for free, and in only three months, simply by changing your lifestyle.
So, knowing that what was once thought impossible can now be accomplished in only a few months may capture our imaginations and be a powerful motivator to make sustainable lifestyle changes. For many people, these are choices worth making—not just to live longer, but also to feel better.
Saturday, January 24, 2009
Some Healthy Recommendations
From: www.health.gov
PHYSICAL ACTIVITY
Key Recommendations
Engage in regular physical activity and reduce sedentary activities to promote health, psychological well-being, and a healthy body weight.
To reduce the risk of chronic disease in adulthood: Engage in at least 30 minutes of moderate-intensity physical activity, above usual activity, at work or home on most days of the week.
For most people, greater health benefits can be obtained by engaging in physical activity of more vigorous intensity or longer duration.
To help manage body weight and prevent gradual, unhealthy body weight gain in adulthood: Engage in approximately 60 minutes of moderate- to vigorous-intensity activity on most days of the week while not exceeding caloric intake requirements.
To sustain weight loss in adulthood: Participate in at least 60 to 90 minutes of daily moderate-intensity physical activity while not exceeding caloric intake requirements. Some people may need to consult with a healthcare provider before participating in this level of activity.
Achieve physical fitness by including cardiovascular conditioning, stretching exercises for flexibility, and resistance exercises or calisthenics for muscle strength and endurance.
Key Recommendations for Specific Population Groups
Children and adolescents. Engage in at least 60 minutes of physical activity on most, preferably all, days of the week.
Pregnant women. In the absence of medical or obstetric complications, incorporate 30 minutes or more of moderate-intensity physical activity on most, if not all, days of the week. Avoid activities with a high risk of falling or abdominal trauma.
Breastfeeding women. Be aware that neither acute nor regular exercise adversely affects the mother's ability to successfully breastfeed.
Older adults. Participate in regular physical activity to reduce functional declines associated with aging and to achieve the other benefits of physical activity identified for all adults.
FOOD GROUPS TO ENCOURAGE
Key Recommendations
Consume a sufficient amount of fruits and vegetables while staying within energy needs. Two cups of fruit and 21/2 cups of vegetables per day are recommended for a reference 2,000-calorie intake, with higher or lower amounts depending on the calorie level.
Choose a variety of fruits and vegetables each day. In particular, select from all five vegetable subgroups (dark green, orange, legumes, starchy vegetables, and other vegetables) several times a week.
Consume 3 or more ounce-equivalents of whole-grain products per day, with the rest of the recommended grains coming from enriched or whole-grain products. In general, at least half the grains should come from whole grains.
Consume 3 cups per day of fat-free or low-fat milk or equivalent milk products.
Key Recommendations for Specific Population Groups
Children and adolescents. Consume whole-grain products often; at least half the grains should be whole grains. Children 2 to 8 years should consume 2 cups per day of fat-free or low-fat milk or equivalent milk products. Children 9 years of age and older should consume 3 cups per day of fat-free or low-fat milk or equivalent milk products.
FATS
Key Recommendations
Consume less than 10 percent of calories from saturated fatty acids and less than 300 mg/day of cholesterol, and keep trans fatty acid consumption as low as possible.
Keep total fat intake between 20 to 35 percent of calories, with most fats coming from sources of polyunsaturated and monounsaturated fatty acids, such as fish, nuts, and vegetable oils.
When selecting and preparing meat, poultry, dry beans, and milk or milk products, make choices that are lean, low-fat, or fat-free.
Limit intake of fats and oils high in saturated and/or trans fatty acids, and choose products low in such fats and oils.
Key Recommendations for Specific Population Groups
Children and adolescents. Keep total fat intake between 30 to 35 percent of calories for children 2 to 3 years of age and between 25 to 35 percent of calories for children and adolescents 4 to 18 years of age, with most fats coming from sources of polyunsaturated and monounsaturated fatty acids, such as fish, nuts, and vegetable oils.
CARBOHYDRATES
Key Recommendations
Choose fiber-rich fruits, vegetables, and whole grains often.
Choose and prepare foods and beverages with little added sugars or caloric sweeteners, such as amounts suggested by the USDA Food Guide and the DASH Eating Plan.
Reduce the incidence of dental caries by practicing good oral hygiene and consuming sugar- and starch-containing foods and beverages less frequently.
SODIUM AND POTASSIUM
Key Recommendations
Consume less than 2,300 mg (approximately 1 tsp of salt) of sodium per day.
Choose and prepare foods with little salt. At the same time, consume potassium-rich foods, such as fruits and vegetables.
Key Recommendations for Specific Population Groups
Individuals with hypertension, blacks, and middle-aged and older adults. Aim to consume no more than 1,500 mg of sodium per day, and meet the potassium recommendation (4,700 mg/day) with food.
ALCOHOLIC BEVERAGES
Key Recommendations
Those who choose to drink alcoholic beverages should do so sensibly and in moderation—defined as the consumption of up to one drink per day for women and up to two drinks per day for men.
Alcoholic beverages should not be consumed by some individuals, including those who cannot restrict their alcohol intake, women of childbearing age who may become pregnant, pregnant and lactating women, children and adolescents, individuals taking medications that can interact with alcohol, and those with specific medical conditions.
Alcoholic beverages should be avoided by individuals engaging in activities that require attention, skill, or coordination, such as driving or operating machinery.
PHYSICAL ACTIVITY
Key Recommendations
Engage in regular physical activity and reduce sedentary activities to promote health, psychological well-being, and a healthy body weight.
To reduce the risk of chronic disease in adulthood: Engage in at least 30 minutes of moderate-intensity physical activity, above usual activity, at work or home on most days of the week.
For most people, greater health benefits can be obtained by engaging in physical activity of more vigorous intensity or longer duration.
To help manage body weight and prevent gradual, unhealthy body weight gain in adulthood: Engage in approximately 60 minutes of moderate- to vigorous-intensity activity on most days of the week while not exceeding caloric intake requirements.
To sustain weight loss in adulthood: Participate in at least 60 to 90 minutes of daily moderate-intensity physical activity while not exceeding caloric intake requirements. Some people may need to consult with a healthcare provider before participating in this level of activity.
Achieve physical fitness by including cardiovascular conditioning, stretching exercises for flexibility, and resistance exercises or calisthenics for muscle strength and endurance.
Key Recommendations for Specific Population Groups
Children and adolescents. Engage in at least 60 minutes of physical activity on most, preferably all, days of the week.
Pregnant women. In the absence of medical or obstetric complications, incorporate 30 minutes or more of moderate-intensity physical activity on most, if not all, days of the week. Avoid activities with a high risk of falling or abdominal trauma.
Breastfeeding women. Be aware that neither acute nor regular exercise adversely affects the mother's ability to successfully breastfeed.
Older adults. Participate in regular physical activity to reduce functional declines associated with aging and to achieve the other benefits of physical activity identified for all adults.
FOOD GROUPS TO ENCOURAGE
Key Recommendations
Consume a sufficient amount of fruits and vegetables while staying within energy needs. Two cups of fruit and 21/2 cups of vegetables per day are recommended for a reference 2,000-calorie intake, with higher or lower amounts depending on the calorie level.
Choose a variety of fruits and vegetables each day. In particular, select from all five vegetable subgroups (dark green, orange, legumes, starchy vegetables, and other vegetables) several times a week.
Consume 3 or more ounce-equivalents of whole-grain products per day, with the rest of the recommended grains coming from enriched or whole-grain products. In general, at least half the grains should come from whole grains.
Consume 3 cups per day of fat-free or low-fat milk or equivalent milk products.
Key Recommendations for Specific Population Groups
Children and adolescents. Consume whole-grain products often; at least half the grains should be whole grains. Children 2 to 8 years should consume 2 cups per day of fat-free or low-fat milk or equivalent milk products. Children 9 years of age and older should consume 3 cups per day of fat-free or low-fat milk or equivalent milk products.
FATS
Key Recommendations
Consume less than 10 percent of calories from saturated fatty acids and less than 300 mg/day of cholesterol, and keep trans fatty acid consumption as low as possible.
Keep total fat intake between 20 to 35 percent of calories, with most fats coming from sources of polyunsaturated and monounsaturated fatty acids, such as fish, nuts, and vegetable oils.
When selecting and preparing meat, poultry, dry beans, and milk or milk products, make choices that are lean, low-fat, or fat-free.
Limit intake of fats and oils high in saturated and/or trans fatty acids, and choose products low in such fats and oils.
Key Recommendations for Specific Population Groups
Children and adolescents. Keep total fat intake between 30 to 35 percent of calories for children 2 to 3 years of age and between 25 to 35 percent of calories for children and adolescents 4 to 18 years of age, with most fats coming from sources of polyunsaturated and monounsaturated fatty acids, such as fish, nuts, and vegetable oils.
CARBOHYDRATES
Key Recommendations
Choose fiber-rich fruits, vegetables, and whole grains often.
Choose and prepare foods and beverages with little added sugars or caloric sweeteners, such as amounts suggested by the USDA Food Guide and the DASH Eating Plan.
Reduce the incidence of dental caries by practicing good oral hygiene and consuming sugar- and starch-containing foods and beverages less frequently.
SODIUM AND POTASSIUM
Key Recommendations
Consume less than 2,300 mg (approximately 1 tsp of salt) of sodium per day.
Choose and prepare foods with little salt. At the same time, consume potassium-rich foods, such as fruits and vegetables.
Key Recommendations for Specific Population Groups
Individuals with hypertension, blacks, and middle-aged and older adults. Aim to consume no more than 1,500 mg of sodium per day, and meet the potassium recommendation (4,700 mg/day) with food.
ALCOHOLIC BEVERAGES
Key Recommendations
Those who choose to drink alcoholic beverages should do so sensibly and in moderation—defined as the consumption of up to one drink per day for women and up to two drinks per day for men.
Alcoholic beverages should not be consumed by some individuals, including those who cannot restrict their alcohol intake, women of childbearing age who may become pregnant, pregnant and lactating women, children and adolescents, individuals taking medications that can interact with alcohol, and those with specific medical conditions.
Alcoholic beverages should be avoided by individuals engaging in activities that require attention, skill, or coordination, such as driving or operating machinery.
Mediterranean Diet
From: www.americanheart.org
What is the "Mediterranean" diet?
There's no one "Mediterranean" diet. At least 16 countries border the Mediterranean Sea. Diets vary between these countries and also between regions within a country. Many differences in culture, ethnic background, religion, economy and agricultural production result in different diets. But the common Mediterranean dietary pattern has these characteristics:
high consumption of fruits, vegetables, bread and other cereals, potatoes, beans, nuts and seeds
olive oil is an important monounsaturated fat source dairy products,
fish and poultry are consumed in low to moderate amounts, and little red meat is eaten
eggs are consumed zero to four times a week
wine is consumed in low to moderate amounts
Does a Mediterranean-style diet follow American Heart Association dietary recommendations?
Mediterranean-style diets are often close to our dietary recommendations, but they don’t follow them exactly. In general, the diets of Mediterranean peoples contain a relatively high percentage of calories from fat. This is thought to contribute to the increasing obesity in these countries, which is becoming a concern.
People who follow the average Mediterranean diet eat less saturated fat than those who eat the average American diet. In fact, saturated fat consumption is well within our dietary guidelines.
More than half the fat calories in a Mediterranean diet come from monounsaturated fats (mainly from olive oil). Monounsaturated fat doesn't raise blood cholesterol levels the way saturated fat does.
The incidence of heart disease in Mediterranean countries is lower than in the United States. Death rates are lower, too. But this may not be entirely due to the diet. Lifestyle factors (such as more physical activity and extended social support systems) may also play a part.
Before advising people to follow a Mediterranean diet, we need more studies to find out whether the diet itself or other lifestyle factors account for the lower deaths from heart disease. See the Lyon Diet Heart Study entry in this Guide for more information.
Related AHA publications:
Easy Food Tips for Heart-Healthy Eating (also in Spanish)
"How Can I Cook Healthfully?" and "How Do I Follow a Low-Fat Diet?" in Answers By Heart kit (also in Spanish kit) See also:Dietary Recommendations for Healthy ChildrenFatFats and OilsMeat, Poultry and FishMilk ProductsObesity and OverweightOverweight in ChildrenStep I , Step II and TLC DietsVegetables and FruitsVegetarian Diets
What is the "Mediterranean" diet?
There's no one "Mediterranean" diet. At least 16 countries border the Mediterranean Sea. Diets vary between these countries and also between regions within a country. Many differences in culture, ethnic background, religion, economy and agricultural production result in different diets. But the common Mediterranean dietary pattern has these characteristics:
high consumption of fruits, vegetables, bread and other cereals, potatoes, beans, nuts and seeds
olive oil is an important monounsaturated fat source dairy products,
fish and poultry are consumed in low to moderate amounts, and little red meat is eaten
eggs are consumed zero to four times a week
wine is consumed in low to moderate amounts
Does a Mediterranean-style diet follow American Heart Association dietary recommendations?
Mediterranean-style diets are often close to our dietary recommendations, but they don’t follow them exactly. In general, the diets of Mediterranean peoples contain a relatively high percentage of calories from fat. This is thought to contribute to the increasing obesity in these countries, which is becoming a concern.
People who follow the average Mediterranean diet eat less saturated fat than those who eat the average American diet. In fact, saturated fat consumption is well within our dietary guidelines.
More than half the fat calories in a Mediterranean diet come from monounsaturated fats (mainly from olive oil). Monounsaturated fat doesn't raise blood cholesterol levels the way saturated fat does.
The incidence of heart disease in Mediterranean countries is lower than in the United States. Death rates are lower, too. But this may not be entirely due to the diet. Lifestyle factors (such as more physical activity and extended social support systems) may also play a part.
Before advising people to follow a Mediterranean diet, we need more studies to find out whether the diet itself or other lifestyle factors account for the lower deaths from heart disease. See the Lyon Diet Heart Study entry in this Guide for more information.
Related AHA publications:
Easy Food Tips for Heart-Healthy Eating (also in Spanish)
"How Can I Cook Healthfully?" and "How Do I Follow a Low-Fat Diet?" in Answers By Heart kit (also in Spanish kit) See also:Dietary Recommendations for Healthy ChildrenFatFats and OilsMeat, Poultry and FishMilk ProductsObesity and OverweightOverweight in ChildrenStep I , Step II and TLC DietsVegetables and FruitsVegetarian Diets
Low-Carbohydrate Diet May Treat Obesity and Diabetes
From: www.newsmax.com
A low-carbohydrate diet may help treat obesity and diabetes say researchers at UT Southwestern Medical Center. A clinical study found that people on low-carbohydrate diets burn more liver fat than those on low-calorie diets, therefore fighting diseases such as diabetes, insulin resistance and nonalcoholic fatty liver disease.
“Instead of looking at drugs to combat obesity and the diseases that stem from it, maybe optimizing diet can not only manage and treat these diseases, but also prevent them,” said Dr. Jeffrey Browning, assistant professor in the UT Southwestern Advanced Imaging Research Center and of internal medicine at the medical center.
Glucose (a form of sugar) and fat are sources of energy that are metabolized in the liver and used as energy by the body. Glucose can be made from lactate, amino acids or glycerol. Too much fat in the liver can lead to nonalcoholic fatty liver disease (NAFLD) a condition that may affect as many as a third of all American adults. NAFLD is linked to metabolic disorders such as insulin resistance and diabetes. It can also lead to inflammation of the liver, cirrhosis and liver cancer.
Researchers gave overweight or obese patients either a low-calorie or low-carbohydrate diet. After two weeks, they used imaging techniques to analyze what techniques the body used to make glucose.
“We saw a dramatic change in where and how the liver was producing glucose, depending on diet,” said Dr. Browning, the study’s lead author. Those on the low-carbohydrate diet produced more glucose from lactate or amino acids than those on a low-calorie diet. Those on low-calorie diets got about 40 percent of their glucose from glycogen, but those on low-carbohydrate diets got only about 20 percent of their glucose from glycogen. Instead, low-carb dieters burned liver fat for energy.
“Energy production is expensive for the liver,” said Dr. Browning. “It appears that for the people on a low-carbohydrate diet, in order to meet that expense, their livers have to burn excess fat.
Results also indicate that those on low-carbohydrate diets increased the amount of fat burned throughout their entire bodies.
Even though the study wasn’t designed to determine which diets worked best to control weight, patients on the low-carb diet lost almost twice as much weight as those on a low- calorie diet.
Editor's Note:
Diabetes is Epidemic. Protect Yourself
A low-carbohydrate diet may help treat obesity and diabetes say researchers at UT Southwestern Medical Center. A clinical study found that people on low-carbohydrate diets burn more liver fat than those on low-calorie diets, therefore fighting diseases such as diabetes, insulin resistance and nonalcoholic fatty liver disease.
“Instead of looking at drugs to combat obesity and the diseases that stem from it, maybe optimizing diet can not only manage and treat these diseases, but also prevent them,” said Dr. Jeffrey Browning, assistant professor in the UT Southwestern Advanced Imaging Research Center and of internal medicine at the medical center.
Glucose (a form of sugar) and fat are sources of energy that are metabolized in the liver and used as energy by the body. Glucose can be made from lactate, amino acids or glycerol. Too much fat in the liver can lead to nonalcoholic fatty liver disease (NAFLD) a condition that may affect as many as a third of all American adults. NAFLD is linked to metabolic disorders such as insulin resistance and diabetes. It can also lead to inflammation of the liver, cirrhosis and liver cancer.
Researchers gave overweight or obese patients either a low-calorie or low-carbohydrate diet. After two weeks, they used imaging techniques to analyze what techniques the body used to make glucose.
“We saw a dramatic change in where and how the liver was producing glucose, depending on diet,” said Dr. Browning, the study’s lead author. Those on the low-carbohydrate diet produced more glucose from lactate or amino acids than those on a low-calorie diet. Those on low-calorie diets got about 40 percent of their glucose from glycogen, but those on low-carbohydrate diets got only about 20 percent of their glucose from glycogen. Instead, low-carb dieters burned liver fat for energy.
“Energy production is expensive for the liver,” said Dr. Browning. “It appears that for the people on a low-carbohydrate diet, in order to meet that expense, their livers have to burn excess fat.
Results also indicate that those on low-carbohydrate diets increased the amount of fat burned throughout their entire bodies.
Even though the study wasn’t designed to determine which diets worked best to control weight, patients on the low-carb diet lost almost twice as much weight as those on a low- calorie diet.
Editor's Note:
Diabetes is Epidemic. Protect Yourself
Tuesday, January 20, 2009
Very low Fat and Cholesterol Diet
From: http://www.heartattackproof.com/
I don’t want my patients to pour a single thimbleful of gasoline on the fire. Stopping the gasoline puts out the fire. Reforming the way you eat will end the heart disease.Here are the rules of my program in their simplest form:
• You may not eat anything with a mother or a face (no meat, poultry, or fish).
• You cannot eat dairy products.
• You must not consume oil of any kind—not a drop. (Yes, you devotees of the Mediterranean Diet, that includes olive oil, as I’ll explain in Chapter 10.)
• Generally, you cannot eat nuts or avocados.
You can eat a wonderful variety of delicious, nutrient-dense foods:•
*All vegetables except avocado. Leafy green vegetables, root vegetables, veggies that are red, green, purple, orange, and yellowand everything in between
• All legumes—beans, peas, and lentils of all varieties.
• All whole grains and products, such as bread and pasta, that are made from them—as long as they do not contain added fats.
• All fruits.
I don’t want my patients to pour a single thimbleful of gasoline on the fire. Stopping the gasoline puts out the fire. Reforming the way you eat will end the heart disease.Here are the rules of my program in their simplest form:
• You may not eat anything with a mother or a face (no meat, poultry, or fish).
• You cannot eat dairy products.
• You must not consume oil of any kind—not a drop. (Yes, you devotees of the Mediterranean Diet, that includes olive oil, as I’ll explain in Chapter 10.)
• Generally, you cannot eat nuts or avocados.
You can eat a wonderful variety of delicious, nutrient-dense foods:•
*All vegetables except avocado. Leafy green vegetables, root vegetables, veggies that are red, green, purple, orange, and yellowand everything in between
• All legumes—beans, peas, and lentils of all varieties.
• All whole grains and products, such as bread and pasta, that are made from them—as long as they do not contain added fats.
• All fruits.
A Strategy to Arrest and Reverse Coronary Artery Disease: A 5-Year Longitudinal Study of a Single Physician's Practice
From: http://www.heartattackproof.com/
A Strategy to Arrest and Reverse Coronary Artery Disease: A 5-Year Longitudinal Study of a Single Physician's PracticeCaldwell B. Esselstyn, Jr, MD; Stephen G. Ellis, MD;Sharon V. Medendorp, MPH; and Timothy D. Crowe
Methods Results Discussion Conclusions References
Background. Animal experiments and epidemiological studies have suggested that coronary disease could be prevented, arrested, or even reversed by maintaining total serum cholesterol levels below 150 mg/dL (3.88 mmol/ L). In 1985, we began to study how effective one physician could be in helping patients achieve this cholesterol level and what the associated effect of achieving and maintaining this cholesterol level has on coronary disease.
Methods. The study included 22 patients with angiographically documented, severe coronary artery disease that was not immediately life threatening. These patients took cholesterol-lowering drugs and followed a diet that derived no more than 10% of its calories from fat. Disease progression was measured by coronary angiography and quantified with the percent diameter stenosis and minimal lumen diameter methods. Serum cholesterol was measured biweekly for 5 years and monthly thereafter.
Results. Of the 22 participants, 5 dropped out within 2 years, and 17 maintained the diet, 11 of whom completed a mean of 5.5 years of follow-up. All 11 of these participants reduced their cholesterol level from a mean baseline of 246 mg/dL (6.36 mmol/L) to below 150mg/dL (3.88 mmol/L). Lesion analysis by percent stenosis showed that of 25 lesions, 11 regressed and 14 remained stable. Mean arterial stenosis decreased from 53.4% to 46.2% (estimated decrease=7%; 95% confidence interval [CI], 3.3 to 10.7, P<.05). Analysis by minimal lumen diameter of 25 lesions fotind that 6 regressed, 14 remained stable, and 5 progressed. Mean lumen diameter increased from 1.3 mm to 1.4 mm (estimated in crease=0.08 mm; 95% CI, --0.06 to 0.22, P=NS). Disease was clinically arrested in all 11 participants, and none had new infarctions. Among the 11 remaining patients after 10 years, six continued the diet and had no further coronary events, whereas the five dropouts who resumed their pre-study diet reported 10 coronary events. Conclusions. A physician can influence patients in the decision to adopt a very low-fat diet that, combined with lipid-lowering drugs, can reduce cholesterol levels to below150 mg/dL and uniformly result in the arrest or reversal of coronary artery disease. Key words. Coronary disease; cholesterol; nutrition; atherosclerosis; preventive medicine. (J Earn Pract 1995; 41:560-568)
By the mid-1980s, experimental studies on animals and epidemiological studies had indicated that total serum cholesterol levels below 150 mg/dL (3.88 mmol/L)were associated with the absence of atherosclerotic heart disease and with possible arrest and even reversal of the effects of heart disease."2 It was also evident that very low-fat diets, with and without drugs, could reduce progression and achieve partial regression of coronary artery disease in humans.3-'5
These studies caused one of the authors (C.B.E) to rethink the treatment of heart disease, as well as his own lifestyle. Aware that medical, angiographic, and surgical interventions were treating only the symptoms of heart disease and believing that a fundamentally different approach to treatment was necessary, he identified through referrals a number of heart patients willing to adopt a program of major dietary change and to be followed for several years so that the effects of the regimen could be documented. This article describes the medical changes that occurred in these participants after maintaining a very low-fat diet over several years. It presents the results of an exploratory study on what a single physician can accomplish with his or her patients, without additional funding, expensive interventions, or a large medical infrastructure.
A Strategy to Arrest and Reverse Coronary Artery Disease: A 5-Year Longitudinal Study of a Single Physician's PracticeCaldwell B. Esselstyn, Jr, MD; Stephen G. Ellis, MD;Sharon V. Medendorp, MPH; and Timothy D. Crowe
Methods Results Discussion Conclusions References
Background. Animal experiments and epidemiological studies have suggested that coronary disease could be prevented, arrested, or even reversed by maintaining total serum cholesterol levels below 150 mg/dL (3.88 mmol/ L). In 1985, we began to study how effective one physician could be in helping patients achieve this cholesterol level and what the associated effect of achieving and maintaining this cholesterol level has on coronary disease.
Methods. The study included 22 patients with angiographically documented, severe coronary artery disease that was not immediately life threatening. These patients took cholesterol-lowering drugs and followed a diet that derived no more than 10% of its calories from fat. Disease progression was measured by coronary angiography and quantified with the percent diameter stenosis and minimal lumen diameter methods. Serum cholesterol was measured biweekly for 5 years and monthly thereafter.
Results. Of the 22 participants, 5 dropped out within 2 years, and 17 maintained the diet, 11 of whom completed a mean of 5.5 years of follow-up. All 11 of these participants reduced their cholesterol level from a mean baseline of 246 mg/dL (6.36 mmol/L) to below 150mg/dL (3.88 mmol/L). Lesion analysis by percent stenosis showed that of 25 lesions, 11 regressed and 14 remained stable. Mean arterial stenosis decreased from 53.4% to 46.2% (estimated decrease=7%; 95% confidence interval [CI], 3.3 to 10.7, P<.05). Analysis by minimal lumen diameter of 25 lesions fotind that 6 regressed, 14 remained stable, and 5 progressed. Mean lumen diameter increased from 1.3 mm to 1.4 mm (estimated in crease=0.08 mm; 95% CI, --0.06 to 0.22, P=NS). Disease was clinically arrested in all 11 participants, and none had new infarctions. Among the 11 remaining patients after 10 years, six continued the diet and had no further coronary events, whereas the five dropouts who resumed their pre-study diet reported 10 coronary events. Conclusions. A physician can influence patients in the decision to adopt a very low-fat diet that, combined with lipid-lowering drugs, can reduce cholesterol levels to below150 mg/dL and uniformly result in the arrest or reversal of coronary artery disease. Key words. Coronary disease; cholesterol; nutrition; atherosclerosis; preventive medicine. (J Earn Pract 1995; 41:560-568)
By the mid-1980s, experimental studies on animals and epidemiological studies had indicated that total serum cholesterol levels below 150 mg/dL (3.88 mmol/L)were associated with the absence of atherosclerotic heart disease and with possible arrest and even reversal of the effects of heart disease."2 It was also evident that very low-fat diets, with and without drugs, could reduce progression and achieve partial regression of coronary artery disease in humans.3-'5
These studies caused one of the authors (C.B.E) to rethink the treatment of heart disease, as well as his own lifestyle. Aware that medical, angiographic, and surgical interventions were treating only the symptoms of heart disease and believing that a fundamentally different approach to treatment was necessary, he identified through referrals a number of heart patients willing to adopt a program of major dietary change and to be followed for several years so that the effects of the regimen could be documented. This article describes the medical changes that occurred in these participants after maintaining a very low-fat diet over several years. It presents the results of an exploratory study on what a single physician can accomplish with his or her patients, without additional funding, expensive interventions, or a large medical infrastructure.
Monday, January 12, 2009
Hormone therapy linked to brain shrinkage in older women
http://www.cnn.com/
By Anne Harding
Not too long ago, millions of postmenopausal women were taking estrogen as part of hormone therapy to protect their hearts, prevent cancer, and keep their brains sharp.
Hormone therapy may place older women at a higher risk of heart attack, brain shrinkage and breast cancer.
But two new studies in the journal Neurology show that not only does hormone replacement therapy increase the risk of heart attack, stroke, blood clots, and breast cancer in women over the age of 65, but it also shrinks their brains.
"This is extra-double-triple reason not to go on estrogen after 65," said Dr. Constantine Lyketsos of the Johns Hopkins Bayview Medical Center in East Baltimore, Maryland. Lyketsos, an expert on dementia treatment, was not involved in the research.
Experts say the findings should not be cause for alarm among younger women who are taking estrogen according to the current guidelines.
The U.S. Food and Drug Administration recommends that women who take hormones to treat hot flashes and other menopausal symptoms start doing so as early as possible, at the lowest effective dose, for the shortest time possible. Women who haven't had a hysterectomy need to take a combination of estrogen and progestin, because estrogen alone increases the risk of cancer of the lining of the uterus; women who've had their uterus removed can take estrogen alone.
There is good evidence that for younger women, estrogen can actually help defog the brain, improve mental function, and possibly even protect against Alzheimer's disease decades later, said Dr. Pauline Maki, who runs a research program on steroid hormones' effect on cognitive function at the University of Illinois at Chicago. She was not involved with the new studies.
One of the most plausible explanations for this paradox is the "healthy cell bias of estrogen." In other words, estrogen is good for healthy cells, and bad for unhealthy cells, she explained. In her own research, Maki has shown that women who experience an unusually high number of hot flashes during menopause have worse verbal memory.
"What I think happens is that women's brains during hot flashes, while they're not sleeping as well -- the brain material is still fine," Maki said. "When you introduce estrogen to these women, you're introducing it into a healthy cell, and the results, cognitively, are generally beneficial."
Health.com: How to cope with hot flashes without using estrogen
Older women's brain cells are likely to be in worse shape than younger women's, especially if their mental faculties are already fading.
"The scenario that seems to arise is one where [hormone therapy] at the dose of this trial is harmful to the frailest brains, but perhaps not to the strongest ones," said Giovanni Frisoni, of the National Center for Research and Care of Alzheimer's Disease in Brescia, Italy. Frisoni has studied estrogen's effects on brain volumes, but was not involved in the new research.
The two news studies are offshoots of the Women's Health Initiative Memory Study (WHIMS), which found an increased risk of dementia in women on hormone therapy. WHIMS is a parallel study to the Women's Health Initiative, the landmark clinical trial, which in 2002 found that hormone therapy was hurting some women more than it helped them.
The WHIMS researchers had suspected that the women on hormone therapy would have blood vessel disease in the brain, which can destroy brain tissue by restricting blood flow to cells, leading to mental impairment and resulting in vascular dementia. To investigate, two WHIMS teams examined brain MRI scans from 1,403 women participating in the study.
"Much to our surprise, something else was going on," said Susan Resnick of the National Institute on Aging's Intramural Research Program, who led one of the studies. Two memory-related brain regions, the frontal lobes and the hippocampus, were slightly but definitely smaller among women taking hormones. Health.com: How to age-proof your memory
"These negative effects were really most evident in women who seemed to already be having some low cognitive function and possibly some memory problems," Resnick said.
Among the women with the smallest amount of vascular damage in their brains, she added, hormone therapy had no effect on the volume of these brain regions. Health.com: The best memory boosters for women
The degree of atrophy suggests a small but real increase in the dementia risk, said Resnick. Starting hormone therapy likely accelerated the disease process in already-vulnerable women, she said.
Health Library
MayoClinic.com: Hot flashes-- Minimize discomfort during menopause
MayoClinic.com: Menopause
MayoClinic.com: Hormone therapy-- Is it right for you?
In the second study, Laura Coker of Wake Forest University Health Sciences, in Winston-Salem, North Carolina, and colleagues, found that women taking estrogen and progestin had slightly larger areas of vascular damage in their brains than those on placebo. The difference wasn't significant, making it clear that vascular disease wasn't behind the women's increased dementia risk.
"When this type of hormone therapy is initiated, you get volume loss in these key brain areas, and where there's loss of volume, there's loss of function," said Maki. Health.com: Foods that boost your brain power
Investigators are looking into other formulations of estrogen and progestin, as well as very low doses of the hormones, to see if they might be safer than the formulation and relatively higher dose taken by participants in the Women's Health Study.
In the 1990s, more than half of menopausal women said they had taken hormones at some point, and one-third took them for at least five years. About 38 percent of women ages 50 to 70 were taking hormones, according to surveys at the time.
Prescriptions for the two most commonly prescribed hormone products, Premarin and Prempro, dropped from 61 million prescriptions in 2001 to 21 million in 2004, according to the National Cancer Institute.
By Anne Harding
Not too long ago, millions of postmenopausal women were taking estrogen as part of hormone therapy to protect their hearts, prevent cancer, and keep their brains sharp.
Hormone therapy may place older women at a higher risk of heart attack, brain shrinkage and breast cancer.
But two new studies in the journal Neurology show that not only does hormone replacement therapy increase the risk of heart attack, stroke, blood clots, and breast cancer in women over the age of 65, but it also shrinks their brains.
"This is extra-double-triple reason not to go on estrogen after 65," said Dr. Constantine Lyketsos of the Johns Hopkins Bayview Medical Center in East Baltimore, Maryland. Lyketsos, an expert on dementia treatment, was not involved in the research.
Experts say the findings should not be cause for alarm among younger women who are taking estrogen according to the current guidelines.
The U.S. Food and Drug Administration recommends that women who take hormones to treat hot flashes and other menopausal symptoms start doing so as early as possible, at the lowest effective dose, for the shortest time possible. Women who haven't had a hysterectomy need to take a combination of estrogen and progestin, because estrogen alone increases the risk of cancer of the lining of the uterus; women who've had their uterus removed can take estrogen alone.
There is good evidence that for younger women, estrogen can actually help defog the brain, improve mental function, and possibly even protect against Alzheimer's disease decades later, said Dr. Pauline Maki, who runs a research program on steroid hormones' effect on cognitive function at the University of Illinois at Chicago. She was not involved with the new studies.
One of the most plausible explanations for this paradox is the "healthy cell bias of estrogen." In other words, estrogen is good for healthy cells, and bad for unhealthy cells, she explained. In her own research, Maki has shown that women who experience an unusually high number of hot flashes during menopause have worse verbal memory.
"What I think happens is that women's brains during hot flashes, while they're not sleeping as well -- the brain material is still fine," Maki said. "When you introduce estrogen to these women, you're introducing it into a healthy cell, and the results, cognitively, are generally beneficial."
Health.com: How to cope with hot flashes without using estrogen
Older women's brain cells are likely to be in worse shape than younger women's, especially if their mental faculties are already fading.
"The scenario that seems to arise is one where [hormone therapy] at the dose of this trial is harmful to the frailest brains, but perhaps not to the strongest ones," said Giovanni Frisoni, of the National Center for Research and Care of Alzheimer's Disease in Brescia, Italy. Frisoni has studied estrogen's effects on brain volumes, but was not involved in the new research.
The two news studies are offshoots of the Women's Health Initiative Memory Study (WHIMS), which found an increased risk of dementia in women on hormone therapy. WHIMS is a parallel study to the Women's Health Initiative, the landmark clinical trial, which in 2002 found that hormone therapy was hurting some women more than it helped them.
The WHIMS researchers had suspected that the women on hormone therapy would have blood vessel disease in the brain, which can destroy brain tissue by restricting blood flow to cells, leading to mental impairment and resulting in vascular dementia. To investigate, two WHIMS teams examined brain MRI scans from 1,403 women participating in the study.
"Much to our surprise, something else was going on," said Susan Resnick of the National Institute on Aging's Intramural Research Program, who led one of the studies. Two memory-related brain regions, the frontal lobes and the hippocampus, were slightly but definitely smaller among women taking hormones. Health.com: How to age-proof your memory
"These negative effects were really most evident in women who seemed to already be having some low cognitive function and possibly some memory problems," Resnick said.
Among the women with the smallest amount of vascular damage in their brains, she added, hormone therapy had no effect on the volume of these brain regions. Health.com: The best memory boosters for women
The degree of atrophy suggests a small but real increase in the dementia risk, said Resnick. Starting hormone therapy likely accelerated the disease process in already-vulnerable women, she said.
Health Library
MayoClinic.com: Hot flashes-- Minimize discomfort during menopause
MayoClinic.com: Menopause
MayoClinic.com: Hormone therapy-- Is it right for you?
In the second study, Laura Coker of Wake Forest University Health Sciences, in Winston-Salem, North Carolina, and colleagues, found that women taking estrogen and progestin had slightly larger areas of vascular damage in their brains than those on placebo. The difference wasn't significant, making it clear that vascular disease wasn't behind the women's increased dementia risk.
"When this type of hormone therapy is initiated, you get volume loss in these key brain areas, and where there's loss of volume, there's loss of function," said Maki. Health.com: Foods that boost your brain power
Investigators are looking into other formulations of estrogen and progestin, as well as very low doses of the hormones, to see if they might be safer than the formulation and relatively higher dose taken by participants in the Women's Health Study.
In the 1990s, more than half of menopausal women said they had taken hormones at some point, and one-third took them for at least five years. About 38 percent of women ages 50 to 70 were taking hormones, according to surveys at the time.
Prescriptions for the two most commonly prescribed hormone products, Premarin and Prempro, dropped from 61 million prescriptions in 2001 to 21 million in 2004, according to the National Cancer Institute.
Thursday, January 1, 2009
Approach to the Patient with Menopausal Symptoms
From: http://jcem.endojournals.org/
By: Kathryn Ann Martin and JoAnn E. Manson
Reproductive Endocrine Unit (K.A.M.), Department of Medicine, Massachusetts General Hospital, Harvard Medical School Boston, Massachusetts 02114; and Division of Preventive Medicine (J.E.M.), Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115
Many women experience menopausal symptoms during the menopausal transition and postmenopausal years. Hot flashes, the most common symptom, typically resolve after several years, but for 15–20% of women, they interfere with quality of life. For these women, estrogen therapy, the most effective treatment for hot flashes, should be considered.
The decision to use hormone therapy involves balancing the potential benefits of hormone therapy against its potential risks. Accumulating data suggest that initiation of estrogen many years after menopause is associated with excess coronary risk, whereas initiation soon after menopause is not.
Therefore, most now agree that short-term estrogen therapy, using the lowest effective estrogen dose, is a reasonable option for recently menopausal women with moderate to severe symptoms who are in good cardiovascular health. Short-term therapy is considered to be not more than 4–5 yr because symptoms diminish after several years, whereas the risk of breast cancer increases with longer duration of hormone therapy.
A minority of women may need long-term therapy for severe, persistent vasomotor symptoms after stopping hormone therapy. However, these women should first undergo trials of nonhormonal options such as gabapentin, selective serotonin reuptake inhibitors, or serotonin norepinephrine reuptake inhibitors, returning to estrogen only if these alternatives are ineffective or cause significant side effects.
Low-dose vaginal estrogens are highly effective for genitourinary atrophy symptoms, with minimal systemic absorption and endometrial effects.
By: Kathryn Ann Martin and JoAnn E. Manson
Reproductive Endocrine Unit (K.A.M.), Department of Medicine, Massachusetts General Hospital, Harvard Medical School Boston, Massachusetts 02114; and Division of Preventive Medicine (J.E.M.), Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115
Many women experience menopausal symptoms during the menopausal transition and postmenopausal years. Hot flashes, the most common symptom, typically resolve after several years, but for 15–20% of women, they interfere with quality of life. For these women, estrogen therapy, the most effective treatment for hot flashes, should be considered.
The decision to use hormone therapy involves balancing the potential benefits of hormone therapy against its potential risks. Accumulating data suggest that initiation of estrogen many years after menopause is associated with excess coronary risk, whereas initiation soon after menopause is not.
Therefore, most now agree that short-term estrogen therapy, using the lowest effective estrogen dose, is a reasonable option for recently menopausal women with moderate to severe symptoms who are in good cardiovascular health. Short-term therapy is considered to be not more than 4–5 yr because symptoms diminish after several years, whereas the risk of breast cancer increases with longer duration of hormone therapy.
A minority of women may need long-term therapy for severe, persistent vasomotor symptoms after stopping hormone therapy. However, these women should first undergo trials of nonhormonal options such as gabapentin, selective serotonin reuptake inhibitors, or serotonin norepinephrine reuptake inhibitors, returning to estrogen only if these alternatives are ineffective or cause significant side effects.
Low-dose vaginal estrogens are highly effective for genitourinary atrophy symptoms, with minimal systemic absorption and endometrial effects.
Blood Sugar Control Linked to Memory Decline
From: www.nytimes.com
By RONI CARYN RABIN
Published: December 31, 2008
Spikes in blood sugar can take a toll on memory by affecting the dentate gyrus, an area of the brain within the hippocampus that helps form memories, a new study reports.
Researchers said the effects can be seen even when levels of blood sugar, or glucose, are only moderately elevated, a finding that may help explain normal age-related cognitive decline, since glucose regulation worsens with age.
The study, by researchers at Columbia University Medical Center and funded in part by the National Institute on Aging, was published in the December issue of Annals of Neurology.
“If we conclude this is underlying normal age-related cognitive decline, then it affects all of us,” said lead investigator Dr. Scott Small, associate professor of neurology at Columbia University Medical Center. The ability to regulate glucose starts deteriorating by the third or fourth decade of life, he added.
Since glucose regulation is improved with physical activity, Dr. Small said, “We have a behavioral recommendation — physical exercise.”
In the study, researchers used high-resolution functional magnetic resonance imaging to map brain regions in 240 elderly subjects. They found a correlation between elevated blood glucose levels and reduced cerebral blood volume, or blood flow, in the dentate gyrus, an indication of reduced metabolic activity and function in that region of the brain.
By manipulating blood sugar levels in mice and monkeys, researchers said, they tried to confirm a cause-and-effect relationship between the glucose spikes and the reduced blood volume, Dr. Small said.
Bruce S. McEwen, who heads the neuroendocrinology lab at Rockefeller University in New York and was not involved in the research, said the study’s findings were “compelling,” with important implications not just for the elderly but for the growing number of overweight children and teens at risk of Type 2 diabetes.
“When we think about diabetes, we think about heart disease and all the consequences for the rest of the body, but we usually don’t think about the brain,” he said. “This is something we’ve got to be really worried about. We need to think about their ultimate risks not only for cardiovascular disease and metabolic disorders, but also about their cognitive skills, and whether they will be able to keep up with the demands of education and a fast-paced complex society. That’s the part that scares the heck out of me.”
Previous observational studies have shown that physical activity reduces the risk of cognitive decline, and studies have also found that diabetes increases the risk of dementia. Earlier studies had also found a link between Type 2 diabetes and dysfunction in the dentate gyrus.
Sheri Colberg-Ochs, an associate professor of exercise science at Old Dominion University in Norfolk, Va., said her research has found that regular exercise, even light physical activity, can offset the potentially negative effects of Type 2 diabetes on cognitive function. It is not clear what the mechanism is, she said, but may have something to do with the effect of insulin.
“This new study is interesting in that it allows for a greater understanding of which region of the hippocampus is likely most affected by poorly controlled diabetes,” she said.
But the elevations in blood glucose seen in the new study are more subtle and would not be considered a disease state, Dr. Small said.
“It’s part of the normal process of aging, much like wrinkling of skin,” he said. “It happens to all of us inexorably, and it worsens progressively across the life span.”
By RONI CARYN RABIN
Published: December 31, 2008
Spikes in blood sugar can take a toll on memory by affecting the dentate gyrus, an area of the brain within the hippocampus that helps form memories, a new study reports.
Researchers said the effects can be seen even when levels of blood sugar, or glucose, are only moderately elevated, a finding that may help explain normal age-related cognitive decline, since glucose regulation worsens with age.
The study, by researchers at Columbia University Medical Center and funded in part by the National Institute on Aging, was published in the December issue of Annals of Neurology.
“If we conclude this is underlying normal age-related cognitive decline, then it affects all of us,” said lead investigator Dr. Scott Small, associate professor of neurology at Columbia University Medical Center. The ability to regulate glucose starts deteriorating by the third or fourth decade of life, he added.
Since glucose regulation is improved with physical activity, Dr. Small said, “We have a behavioral recommendation — physical exercise.”
In the study, researchers used high-resolution functional magnetic resonance imaging to map brain regions in 240 elderly subjects. They found a correlation between elevated blood glucose levels and reduced cerebral blood volume, or blood flow, in the dentate gyrus, an indication of reduced metabolic activity and function in that region of the brain.
By manipulating blood sugar levels in mice and monkeys, researchers said, they tried to confirm a cause-and-effect relationship between the glucose spikes and the reduced blood volume, Dr. Small said.
Bruce S. McEwen, who heads the neuroendocrinology lab at Rockefeller University in New York and was not involved in the research, said the study’s findings were “compelling,” with important implications not just for the elderly but for the growing number of overweight children and teens at risk of Type 2 diabetes.
“When we think about diabetes, we think about heart disease and all the consequences for the rest of the body, but we usually don’t think about the brain,” he said. “This is something we’ve got to be really worried about. We need to think about their ultimate risks not only for cardiovascular disease and metabolic disorders, but also about their cognitive skills, and whether they will be able to keep up with the demands of education and a fast-paced complex society. That’s the part that scares the heck out of me.”
Previous observational studies have shown that physical activity reduces the risk of cognitive decline, and studies have also found that diabetes increases the risk of dementia. Earlier studies had also found a link between Type 2 diabetes and dysfunction in the dentate gyrus.
Sheri Colberg-Ochs, an associate professor of exercise science at Old Dominion University in Norfolk, Va., said her research has found that regular exercise, even light physical activity, can offset the potentially negative effects of Type 2 diabetes on cognitive function. It is not clear what the mechanism is, she said, but may have something to do with the effect of insulin.
“This new study is interesting in that it allows for a greater understanding of which region of the hippocampus is likely most affected by poorly controlled diabetes,” she said.
But the elevations in blood glucose seen in the new study are more subtle and would not be considered a disease state, Dr. Small said.
“It’s part of the normal process of aging, much like wrinkling of skin,” he said. “It happens to all of us inexorably, and it worsens progressively across the life span.”
Subscribe to:
Posts (Atom)